6 - Toronto Notes 2011 - Dermatology

D
Dermatology
Venetia Lo, Farheen MU58alli and Nancy Xi, chapter editors Christophel' Kitamura and Michelle Lam, associate editors Janine Hutson, EBM editor Dr. Perla Lansang, staff editor
Introduction to Skin . . . . . . . . . . . . . . . . . . . . . 2 Skin Anatomy Skin Function Definitions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Primary Morphological Lesions Secondary Morphological Lesions Other Morphological Lesions Patterns and Distribution Differential Diagnoses of Common Presentations . . . . . . . . . . . . . . . . . . . . . . . . . . 4 Common Skin Lesions ................... 6 Cysts Fibrous Lesions Hyperkeratotic Lesions Keloids Pigmented Lesions Vascular Lesions Acneiform Eruptions .................... 12 Acne Vulgaris/Common Acne Perioral Dermatitis Rosacea Dermatitis (Eczema) .................... 14 Asteatotic Dermatitis Atopic Dermatitis Contact Dermatitis Dyshidrotic Dermatitis Nummular Dermatitis Seborrheic Dermatitis Stasis Dermatitis Lichen Simplex Chronicus Papulosquamous Diseases ............... 18 Lichen Planus Pityriasis Rosea Psoriasis Vesiculobullous Diseases ................ 20 Bullous Pemphigoid Dermatitis Herpetiformis Pemphigus Vulgaris Porphyria Cutanea Tarda Drug Eruptions ........................ 22 Drug Hypersensitivity Syndrome Erythema Multiforme (EM) Stevens-Johnson Syndrome (SJS) Toxic Epidermal Necrolysis (TEN) Exanthematous Eruptions Fixed Drug Eruption Photosensitivity Eruptions Serum Sickness-Like Reaction Heritable Disorders . . . . . . . . . . . . . . . . . . . . . 24 Ichthyosis Vulgaris Neurofibromatosis Vitiligo Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25 Bacterial Infections Dermatophytoses Parasitic Infections Viral Infections Yeast Infections Sexually Transmitted Infections Pre-Malignant Skin Conditions ........... 33 Leukoplakia Malignant Skin Tumours ................ 33 Basal Cell Carcinoma (BCC) Cutaneous T-cell Lymphoma Malignant Melanoma (MM) Squamous Cell Carcinoma (SCC) Alopecia (Hair Loss) .................... 36 Hair Growth Non-Scarring (Non-Cicatricial) Alopecia Scarring (Cicatricial) Alopecia Nails and Disorden of the Nail Apparatus .. 38 Nail Plate Changes Surface Changes Colour Changes Nail Fold Changes Skin Manifestations of Systemic Disease ... 39 Autoimmune Disorders Endocrine Disorders HIV-related Malignancy Others Pediatric Exanthems .................... 40 Miscellaneous Lesions .................. 41 Angioedema and Urticaria Erythema Nodosum Pruritus Wounds and Ulcers Common Medications ................... 43 Sunscreens and Preventative Therapy Topical Steroids Dermatologic Therapies References . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46
Toronto Notes 2011
Dermatology Dl
D2 Dermatology
Introduction to Skin
1'oroDio
2011
Introduction to Skin
Skin Anatomy
A
-------------------------------
l.tyen of till Epl-.15 "WomW.. Lte6etli'lg lkrl lulll$"
F"IJira 1. Crass..S.ctian Df the VariaiiS Lly.s Df Skin. Epidarmallll'(llr is datailad in A Skin
divided anatomically into epidermis, dermis, and subcutaneoWJ ti!lsue

epidermiJ
dermiJI - comprised of ronnective tissue divided into two regions:
avascular: receives .its nutrition from the dermal capillariea derived from keratinocytes with the youngest presenting at the 'base' (see layers Figure IA) cells progress from stratum basale to stratum corneum in about four weeks sttatum basale (germlnativum): mitotic figures that give rise to keratinocytes stratum spinosum (prickle cells): junctions in this layer (tonofilament5) give the epidermis i1B strength stratum granulosum: flat cells containing basophlll.c granules which characterize skin stratum lucidum: comprised of transparent layers ofpacked dead cells sttatum corneum: fiat scales of the reaistant protdn keratin other epidermal cells include melanocytes, Langerbans cells, and whl.te blood cells
paplllary: contains numerous caplllarles that supply nubients to the dermis and epidermis reticular: provides a strong structure for skin; consists of collagen bundles woven together along with elastic fibres, fibroblasts, and maaophages
subcutaneous tissue (subdermal) consists primarily ofadipose cells
Skin Appendag81
epidermal in origin; can enend into the dermls include hair, nails, and ClltaneoWI glands
Cutaneous Glands gland- part of pilosebaceoua unit, produces sebum which is secreted into the hair
follicle via the sebaceoWI duct, where It covers the skin surface (protective function) sebum has some antifungal properties found over entire skin surface except palms and soles apoalne sweat gland - apocrine duct empties into hair follicle above sebaceous gland
found in axillae and perineum main function is to produce scent (Le. pheromones) ea:rine sweat gland - not part ofpilosebaceous unit found over entire skin surface except lips, nail beds and glans penis important In temperature regulation via secretl.on of sweat to cool skin surtace
Skin Function
protection due to continuoWI recycling and avascularity of epidermis barrier to: UV radiation, nlechanicallchemi.Cal inSults, pathogens and dehydruion thermal regulation insulation tD maintain body temperature in cool environments, via hair and subcutaneous adipose tissue dissipation of heat in warm environments, via increased activity ofsweat glands and increased blood flow within dermal vascular networks sensation largest sensory organ of the body, with touch, pain, and temperature sensation metabollc function vitamin D synthesis energy storage (mainly in the form of triglyceride&)
Toronto Notes 2011
DefinitiODB
Dermatology D3
Definitions
Primary Morphological Lesions
Definition
an initial lesion that has not been altered by trauma or manipulation and has not regressed macule: flat lesion <1 em patch: flat lesion em papule: elevated, palpable lesion <1 em plaque: elevated, palpable lesion 1 em nodule: deep, palpable lesion <1 em, often dermal or subcutaneous in origin tumour: deep, palpable lesion 1 em vellicle: fluid-filled lesion <1 em bulla: fluid-filled lesion em cyst: a nodule containing semi-solid or fluid material pustule: an elevated lesion containing purulent fluid (white, grey, yellow, green) erosion: a disruption of the skin involving the epidermis alone, heals without scarring ulcer: a disruption ofthe skin that extends into the dermis or deeper; heals with scarring
't'
Descrlle LIISion wllb SCALDA

Size and lurfllce area
Colour (e.g. hyp81Pi!rment8d,
hypopigmented, ertthemltousl
Arrangement (e.g. solitary, linear,
retil:ullted. grouped, herpetiform) Lecion morphology (188 Table 1) Distribution (e.g. dermatomal,
intertriginous, synvnatricaV
asymmllriclll, follicular) Always check hair, 11111ils, mucous membranes llld iltertriginous areas
.....
',
1:111111' "
Sldn Photolypn IFIIzpllllckJ
I'IIIIIDIWI
sw ..,.... ..
SPf pniiCiiln)
SUi
Table 1. Types of Lesions
<1em Dillllllllr
Flat lesion Raised Supelficial Lesion
(e.g. freckle)
:1:1 em Diallllllllr
Wllita
D
Alwlys llllnt. nMr

tins
Patch (e.g. vitiligo)
Wllita Wllill
Alwlys lllln1, ltlulln

Siglltb1111, llaw 1111
Papule (e.g. wart) Nodule (e.g. dermatofibroma) Vesicle (e.g. herpes simplex virus (HSV))
Plaque (e.g. psoriasis) Tumour (e.g. lipoma) Bulla (e.g. bullous pemphigoid)
m
IV
Deep Palpable (dermal or subcutaneous)
I'Hbmwn Sligllt b1111, lullr lin

Blown lllraly!MM,U\1111
Bevated Fluid-filled Lesions
v
VI
Secondary Morphological Lesions

Definition
lllrkbmwn NmrU.,dllrtlln or bllck
-------------------
develop during the evolutionary process of skin disease, or created by manipulation, or due to complication of primary lesion (e.g. rubbing, scratching, infection) crust: dried fluid (serum, blood, or purulent exudate) originating from a lesion (e.g. impetigo) scale; excess keratin (e.g. seborrheic dermatitis) lichenification: thickening of the skin and accentuation of normal skin markings (e.g. chronic atopic dermatitis) fisaure: a linear slit-like cleavage of the skin excoriation: a scratch mark :uresis: pathologic dryness of skin (xeroderma), conjunctiva (xerophthalmia), or mucous membranes atrophy: histological decrease in size and number of cells or tissues, resulting in thinning or depression of the skin
Other Morphological Lesions

comedones: collection of sebum and keratin open comedo (blackhead) closed comedo (whitehead) purpura: extravasation ofblood into dermis resulting in hemorrhagic lesions; non-blanchable petechiae: small pinpoint purpura ehymosa: large flat purpura, "bruise" telangiectasia: dilated superficial blood vessels; blanchable scar: replacement fibrosis of dermis and subcutaneous tissue (hypertrophic or atrophic) wheal: a special form of papule or plaque that is blanchable and transient, formed by edema in the dermis (e.g. urticaria)
D4 Dermatology
Definitions/Differential Diagnoaea of Common Presentations
Toronto Notes 2011
Patterns and Distribution

acral: relating to the hands and feet (e.g. hand, foot and mouth disease)
annular lesions: ring shaped (e.g. granuloma annulare) follicular lesions: involving hair follicles (e.g. folliculitis) guttate lesions: lesions following a "drop-like" pattern (e.g. guttate psoriasis) Koebner phenomenon: isomorphic response, appearance of lesions at an injury site (e.g. molluscum, lichen planus, psoriasis, warts) morbilliform: a maculopapular rash resembling measles reticular lesions: lesions following a net-like pattern (e.g. livedo reticularis) satellite lesions: lesions scattered outside of primary lesion (e.g. candida diaper dermatitis) aerpignousleaions: lesions following a snake-like pattern (e.g. cutaneous larva migrans) target (iri&) lesions: concentric ring lesions, like a dartboard (e.g. erythema multiforme) other descriptive terms: discrete, clustered, linear, confluent, dermatitic, indurated
Differential Diagnoses of Common Presentations

l'$ori1S$iS Xarrthelma kerllosis Basal cell carcinoma Squamous call carcinoma Sebonheic kenrtosis Angulw cheilitis Sabonhaic darmlltilis Solar lentigo Melasma Rosacea Acne Venous lake Herpes labialis
;;
II 1i
i-
...
Spider niMis Malanocytic niMIS Dysplastic niMIS Lichen planus l'$orillsis
Candidiasis Tinea inguinllis Psoriasis
Oermatufibroma
'-----l'$orillsis Lichen simplex chronicus-----.../ '-----Malignant melanoma (in women) '-----Ichthyosis
Status dermllilis-----__,
Venous leg u l c e r - - - - - - " f
Figura Z. Common Lesions Basad on Anatomical Distribution
Toronto Notes 2011
Differential Diagnosea of Common Presentations
Dermatology D5
Table 2. Differential Diagnosis of Common Presenting Proble

Lesion Brawn Macule lnfaclious lniiiiiiiiiiDry Drug/Toxin UV radiation, lentigo,
Misc:lll1111aus
Congenital: spats. congenital nevus, epidennaVjunctional news Neoplasia: lentigo maligna, malignant melanoma. pigmented basel cell carcinoma (BCC) Other: melasma/chloasma ("mask of pragnancyj Vascular: hemangioma, pyogenic granuloma Other: dermatofibroma, miaria rubra
Post-inllammatory hyper-piiJTientation
freckle
Diac111fB Red Papule
Folliculitis Furuncle Scabias
Acne vulgaris Lichen planus Rosacee Psoriasis Urticaria

Denna1itis (atopic, corrtact, nunvnular, seborrtJeic) Discoid lupus lichen planus Psoriasis Acute contact dermatitis Dyshidrotic eczema
Bites/stings
Red Scides
Pityriasis rosea Secondary syphlis
Gold
Neoplastic: mycosis fungoides
Tilea
Vasida
Cat-5cratdl disease Impetigo Viral: HSV, mster, varicella, molluscum, coxsackie Scabias Bulousirrigo
Other: dermatits herplllifcrmis, paqilyria cutanee tanla
Bullae
Acute dermatitis Erythema Multifonne (EM) Stsvan-Johnson Syndrome (SJS) Toxic Epidennal Necrosis (ltN) Systemic ILPJS erythematosus (SLE)
Fixed drug eruption
Autoimmune: bullous pemphi!JJS vulgaris Other: harplllifcrmis, poqilyria cutanea tanla
Pullule
C!lldida Dennatophyte Impetigo Sepsis Varicalla Aspergllosis
Acne vulgaris Rosacee Dyshidllllic dermatitis Pustular folliculitis Pustular psoriasis

Allergic stomatitis EMISJS/TEN lichen planus Seronegatives, SLE Recummt aphthous stomatitis Beh!;et's disease
Acute gannlizud 8Xilllhematous (usually secondary to drug reaction)
Other:
5Uppurativa
Oral Ulctr
CMV
Coxsackie Cryptococcosis HSVJllZV Hill, TB, Sypiilis
Chemotherapy Radiation therapy
Autoimmune: pgus vulgaris Congenital: XXV Hematologic: siclde cell disease Neoplasia: BCC, squamous cell carcinoma (SCC)
Skin Uk:
Plague Syphilis
TB
RA, Slf, vasculitis Ulcanrtiva colitis (pyoderma geniJI!Ilosum)
Tularemia
Autoimmune: necrobiosis lipoidica diabaticorum (e.g. OM) Congenital: XXV Hematologic: siclde cell disease Neoplasia: sec Vascular: artarial, neurotropic, prassura, venous. alilthous, leukoplakia, traumatic
D6 Dermatology
Common Skin Lesions
Toronto Notes 2011
Common Skin Lesions

Cysts
T1ble 3. Cysts
Epidennal Cyst [Sebaceous)
Clinicll Pilar Cyst (nichile11mal) Multiple, hlr'd, varying simd nodules under 1he scalp, lacks centnll punctum
Dennoid Cyst
Most commonly found lllllllenll third of eyebrow or midline under nose
Ganglion Cyst Usualy solilary, rubbery, tnJnslucent; a clear gelatinous viscous ftuid may be axtrudad
Milium
Preseltatilll
Round, yellowlllash coloured, slow growing. mobile, firm, fluctuant, nowle or tumour
1-2 mm superficial,
whit& to yellow
subepidermal papules occuring on eyelids, cheeks, forehead Wrthin pilosebaceous follicles Small epidennoid cyst, primarily arising from pluripotential cells in epidermal oradnaxal epithelium Secondary to blistering. ulceration, trauma, topical corticosteroid atrophy, or cosmetic procedures
Plthophpialagy
Epithelial cells displaced into delmis, epidermal lining becomes filled with ksrlllin and lipid-rich debris May be post-tnJLITIIItic
Thick walled cyst lined with stratified squamous epithelium and filed with dense lanlin ldioplllhic Post-tnJuma
Rare, congenital hamartomas, which arise from inclusion of epidermis along embryonal cleft closure lines, craating athick walled cyst filled with dense ksl'lllil
Cystic lesion that originates from joint or tendon sheath, called B mucous cyst when found on fingertip Associllled with osteoarthritis
Epidemialagy
Most common cuta1eous cyst in youth - mid age
znd most common Rare cutllleous cyst F>M

lfnasal midline, risk of axt8nsion intoCNS
Older age
Any age 40-511% of infants

In nevuborns, 1ponbll8ously molvel in first 4weeks of life
Clinical Couna
Central punctum may Rupture causes rupture (foul, cheesy pain and odour, creamy colour) inflammlllion and produce inflammlllory reaction Increase in siza and number aver time. especially in pregnancy Excise complel!ly before it becomes infected Excision
Stable
Mlniglllllll:
Excision
Drainage :!: steroid injection if painful Compression daly for6weeks Excision if bothersome
Incision and expression of contents Laser ablation and Multiple facial miia responds to topical retinoid therapy
Fibrous Lesions
DERMATOFIBROMA Clinical Presentation button-like, firm dermal papule or nodule, skin-coloured to red-brown colouring majority are asymptomatic but may be pruritic and/or tender site: legs > arms > trunk dimple sign: lateral compression causes dimpling of the lesion Pathophysiology benign tumour due to fibroblast proliferation in the dermis Etiology unknown; often associated with history of minor trauma (e.g. shaving or insect bites) Epidemiology adults, F>M Differential Diagnosis dermatofibrosarcoma protruberans, malignant melanoma, Kaposi's sarcoma. blue nevus
Toronto Notes 2011
Common Skin Lesions
Dermatology D7
Investigations biopsy if diagnosis is uncertain Management no treatment required excision or cryosurgeryifbothersome SKIN TAGS Clinical Presentation small (1-1 0 mm), soft, skin-coloured or darker pedunculated papule, often polypoid sites: eyelids, neck. axillae, inframammary, and groin Pathophysiology benign outgrowth of skin Epidemiology middle-aged and elderly, F>M, obese Differential Diagnosis pedunculated seborrheic keratosis, compound or dermal melanocytic nevus, neurofibroma Management excision, electrodessication, cryosurgery
'. I
..
lldn tap are lcnawn ..

Acrochordon Fibroepilhalial polyps Soft fibromllli Pedunculated lipofibromas Clllaneous papillomas
Hyperkeratotic Lesions
SEBORRHEIC KERATOSIS Clinical Presentation well-demarcated waxy papule/plaque with classic "stuck onD appearance large variety in colour, size and shape over time lesions appear more warty, greasy and pigmented sites: face, trunk, upper extremities (may occur at any site except palms or soles) Pathophysiology very common benign epithelial tumour Epidemiology unusual <30 years old autosomal dominant inheritance Differential Diagnosis malignant melanoma (lentigo maligna, nodular melanoma), melanocytic nevi, pigmented basal cell carcinoma, solar lentigo, spreading pigmented actinic keratosis Investigations biopsy only if diagnosis uncertain Management none required, for cosmetics only liquid nitrogen, curettage ACTINIC KERATOSIS (SOLAR KERATOSIS) Clinical Presentation ill-defined, scaly erythematous papules or plaques on a background of sun damaged skin (solar heliosis) sandpaper-like, gritty sensation felt on palpation sites: areas of sun exposure (face, ears, scalp ifbald, neck, sun exposed limbs) Pathophysiology UV radiation damage to keratinocytes from repeated sun exposure (especially UVB) can develop into squamous cell carcinoma (1-10%)
D8 Dermatology
Common Skin Lesions
Toronto Notes 2011
.....
, ...-----------------,
Epidemiology
common with increasing age, outdoor occupation, M>F skin phototypes I-III (see sidebar, D3), rare in darker skin as melanin is protective
TYPIM of Actinic ICerato- lAICal Erythemato - typical AK leaion Hypartruphic- thickllr, rough papultl pi aqua Clllllneous horn- finn hyparbmotic outgrowth Actinic chaillil - confluant AKa on the lip Pigmented - flat. ten-brown, scaly plaque Spreallng pigmtntlld ProliflndiVI
CanjunctiVIII- pinguecula, pturyuium
Differential Diagnosis
SCC in situ. superficial BCC, seborrheic keratosis, cutaneous lupus erythematosus
Investigations
biopsy lesions that are refractory to treatment
Management
destructive: liquid nitrogen, electrodessication and curettage pharmacotherapy: Efudex (5-fluorouracil) cream for 2-3 weeks, Aldara (imiquimod) cream for 8-10 weeks
KERATOACANTHOMA Clinical Presentation

rapid growing, firm, dome-shaped, erythematous or skin-coloured nodule with central keratin-filled crater, resembling an erupting volcano often spontaneously regresses within a year, leaving a scar sites: sun-exposed skin
Pathophysiology
epithelial neoplasm with atypical keratinocytes in epidermis considered a low grade variant of sec
Etiology
HPV, UV radiation, chemical carcinogens (tar, mineral oil)
Epidemiology
>50 years, rare <20 years
treat as SCC until proven otherwise, hypertrophic solar keratosis, verruca vulgaris
Management
surgical excision
CORNS
.....
.. ,
black speckled central appearance dua to ttnmbosed capillarias. Planter warts destroy dennatoglyphics (apidamnal ridges).
Clinical Presentation firm papule with a central, translucent, cone-shaped, hard keratin core
painful with direct pressure sites: most commonly on dorsolateral fifth toe and dorsal aspects of other toes
Cams VI. W.rts VI. Cilia Cams h11V8 a whitish yellow centrll translucent kllratinous core. Painful with direct pressure. Warts blaed with paring and have a
Pathophysiology
localized hyperkeratosis induced by pressure on hands and feet
Epidemiology
F>M, can be caused by wearing high-heeled shoes with a tapered toe
tinea pedis, plantar warts
Callouses have layers at yellowish kntin FWMiad with parilg. Thare
are no thrombosed capillaries or interruption of apidannal ridges.
Management
relieve pressure with padding or alternate footwear paring, curettage
Toronto Notes 2011
Common Skin Lesions
Dermatology D9
Keloids
Clinical Presentation
firm, shiny, skin-coloured or red-bluish papules/nodules that most often arise from Qltaneous injury (e.g. piercing, surgical scar, acne), but may appear spontaneously extends beyond the margins of the original injury, and may continue to expand in size for years with claw-like extensions can be pruritic and painful sites: earlobes, shoulders, sternum, scapular area
Pathophysiology excessive proliferation of randomly organized collagen fibers following trauma to skin differentiated from a hypertrophic scar which is confined to the borders of the original injury Epidemiology predilection for darker skin M=F, all age groups Management intralesional corticosteroid injections cryotherapy silicone compression
.... .----------------.
Klleldl VI. HypM'II'Opblc Scan Keloln: extend bevond marvins of original injury ike
'.. '
ext111sions
0
ltypartropllic HUI: Confined to
original margins of injury
Pigmented Lesions
Tabla 4. Comparison of Pigmented Lesions
Ephllidel(fnlckll
Clinical l'mentldian Smaii(<Smm)walldemai'CIIIed light brown macules Sites: suiHIXj)Osed skin
Salu LBntiga
(Uv.Spatl
MDngallnSpat
Becbr's Nevus
Hairy, light brown macule/ patch with a papular verruCilus surface Silas: trunk and shouldars Pigmented hamartoma with incraased melanin in basal cells
....
''
stain I
coagulants, staroids, hemosiderin
Wall demarcal8d brown' CongenitaiiJliY-blue black irregular macules macule ccmnonly on Sites: sun.exposed skin lumbosacral area
DDxaf lfn*piFI...... rMIW. PurpUIII (1.g. solar, NOA. anti-
Post-inftamrnatory
Meluma
Increased melanin wilhin Benign melanocytic Ectopic melncytes basallllya" kllratinacytas proliferation in diiTIIillin dermis second!ly to sun epidennal junction due to exposure chronic sun exposure Skin phatotypes I and II
Melanom Find drug 11111ption
Most Cllmmon in Caucasians >40 yea'S Skin phatcrtype
99% occurs in Asian and Aboriginal ilfa1ts
M>F
Often beCilmBS noticeable at puberty

Hairy Cllngsnital melanacytic nevus Hair growth follows onset of pigmentation Cosmalic management (usually too large to remove)
Diagnosis
Junctional nevi Juvenie lentigines
sebonheic keratosis,
solar keratosis
Lsntigo maligna.
Ecc:hyma&i&
Clinical Course andMMBgamant
Laser therapy, shave No treatment required Multiply and dlrtl!n with excisions, ayatherapy sun exposure, fade in
Usually fades in early childhood but may persist into adullthoad
wilter
Sunscreens may prevent the appearance
of new freckles
SEBORRHEIC KERATOSIS (see Hyperkeratotic Lesions section, D7) NEVOMELANOCYTIC NEVI (NMN) (see Table 5) common mole be suspicious of new pigmented lesions in individuals >40 years average number of moles per person: 18-40 3 stages of evolution: junctional NMN: macular; arise at dermal-epidermal junction compound NMN: papular; nevus cells invade the papillary dermis dermal NMN: skin coloured papules (no longer hyperpigmented); nevus cells completely migrate into dermis
DIO Denoatology
Common Skin Lesions

Table 5. Nevomelanocytic Nevi Classification
Type CanQIRillll
Toronto Notes 2011
Alii of Onset
Birth
Clinicll Plwstnbdi111
Hislalagy
MIRIIIIIJient
NMN
Newmel111ocytes in Surgical excision huspiciaus, Sharply demarcated pi!Jnented brown with rep.-/irregular epidermis (dusters) and due ID increased risk of contours coarse han dermis (strands) melanoma Rule aut leptomeningeal involvement an heacVneck Bani!JI neoplasm of pigmentforming news cell Well circumscribed, round, uniformly pigmented maculesf papulas <1.5 em Classified according to of news cells Melanocytes Ill: epidermal junction abova basement membrane Excisianal biopsy required
Acquired
NMN
Early childhood ID age 40 Involute by age60
if an scalp, sales, mucous

membranes, anogenital na, or varied colaurs, borders, bleeding, exposed ID trlluma Same as above
JunctiaMI
NMN
Flat, bordered, uniformy Childhood Majority tan-dark brawn, sharply demarclll:ed progress to smooth macule compound news
Campound
NMN
Any age
Domed, regularly bordered, smooth, Melanocytes Ill: roLild, tan-dark brawn papule epidermal junction; Face, trurt. extremities, scalp migration into dermis NOT found an palms or soles Soft, dome-shaped, skin-calouned ID tarv'brown papules or nodules, often with te1111giectasia Sites: face, neck Melanocytas exclusively in dermis
Same as above
DennaiNMN
Adults
Same as abova
Dpplatic
Childhood
Variegated macule/papule
irregular indistinct rnelanocytes in the basel cell layer >6mm Risk factors: positive family history
NMN
and proliferation of melanocytes extending beyond dermal cornpertment of 1he nevus Often with region of adjacent nasts Dermal or Clllq)Ound newcellular news surroLilded by hypomelanosis, lymphocytes, histocytes
Follow qZ-6 months with colour phatograli!s for changes Excisional biopsy if lasion changing or highly atypical
HaloNMN
First 3 dacadas
Brawn ovaVraund papules surrounded by hypamelanosis Same sites as neocellular news Sponteneous involution 111Q18S$ion of centrally loclll:ad pigmented nevus
Nona required Excision if colour variegated or irregular borders Associated with vitiligo, mlll:a&tatic rnelanama
Childhood 111d lkliformly blue to blue-black late adolescence macule/papule with smooth border <6mm
Pigmented melanocytes Remove if sudden onset and mallllophages in or has chlllged dermis
Vascular Lesions
Table &. Vascular Tumoura Compared to Vascular MaHonnationa
V.Cullr TUIIOUII
Dllfiniti111
l're.ICIIII: Birth
Vascullr M111Drmilli1111
Normal endothelial tumovar 1DD% Ill: bi'lh (nat always obvious) 1:1 Proportionate growth (can expand)
Endothelial Usually postnatal 1:3-1:5 Phases:
M:F
Natural History
lnwkrtilg lnwkrted
HEMANGIOMAS Clinical Presentation is a vascular tumour, defines as benign proliferation of vessels in the dermis is red or blue, nodular and blanches with pressure includes: cavernous hemangioma, capillary/infantile hemangioma, spider hemangioma
Toronto Notes 2011 Table 7. Vascular Tumours

H1111111ioma Capillaryjlnflntie
Common Skin Lesions
Dermatology Dll
Spid Algioma
(Campbell tellngiectalial Central rad arlllriole with slender branches, faintly pulsatile, blancheble face, foraa11115, andhends
!spider llrlwberry
IIMII)
Cllany Angioma (Demoi'JIIn lpDI)

Bright rad to deep IIIIII'DDII, domesheped vascular papules, 1-5 mm Sita: tJUnk Less friable compedto pyogenic granulomas Benign vascular naoplasm
Pyogenic QoanuiORII Bright rad, domeshaped sessile or pecllnculated nodule Sites: fingers, lips, mouth, tJUnk. toe& DDx: glomus tumoW", nollllll' malignant melanoma, noclliii'BCC
Clinh:al Prealllbdion
Sllh. compressible, Congenital racilblue bluish. subcutaneous nodules mass that feels Iiiii! a bag of wonns when palpated Site: anywhere (distribution may indicate underlying cranial abnormality)
sec,
....
,,
Plthaphysiolagy Deeply situated Congenital benign IJ'Oiifaration of thick vascular prolifaration walled blood VliSSals of andotheliallining (consumptive thrombocytopenia if hemangioma enlll'ges rapidyl Can be part of PHACES syndrome
Associated with hyparastrogllic sta111 (e.g. in hepatocelhjll' disease, pregnancy, oral contraceptive pill)
Rapidly developing hamangioma Proliferation of capilaries with erosion of epidennis and neutrophilia
A1pider angiOiflll will blanch when the tip of I papan:lip is applied to 1h; Clll1lr8 of tha la1ion.
......
,,.__________________ ,
Pyovenil: is amisnomer: it i5 neither pyogenic nor Q1111Uiumatou1.
Epideftology
Clinical Coune
Can be congenital Most appear Iller Can ulcenrte Persists, generally do not involute Appears shortly Biter 9 months. increases il size over months, than regresses 511% of lesions resolva spontaneously by 5 years Consider excision f not gone by schoal age. 10% require treatment due to functional impainnent (viSUIII compromise, airway obstruction, high output cardiac fllilura) or cosmesis Propanolal; systemic corticosteroids lnCR!IIse in rurmer overtime
>30 years old Lesions bleed frequently and persist for months
<30 years old
Management
Surgical removal
8ectro or laser Usually no surgery treatment needed Systemic Laser or electrocautery corticosteroids and IN F-a may be for small lesions indicated for rapidly Excision Df large growing lesions lesions if necessii'Y
Surgical excision with histologic exanilation Electrocautery; laser; cryotherapy
VASCULAR MALFORMATIONS 1. Nevus flammeus (Port-wine stain) Clinical Presentation
red to blue macule present at birth that follows a dermatomal distribution, rarely crosses midline most common site: nape of neck
Pathophysiology
congenital vascular malfonnation of dermal capillaries; associated with Sturge Weber syndrome (Vl, V2 distribution)
Management
laser or camouflage (ie. make-up)

2. Nevus simplex (salmon patch) Clinical Presentation
pink-red irregular patches midline macule on glahella known as Angel Kissn; on nuchal region known as stork Bites present in 1/3 of newborns majority regress spontaneously
Pathophysiology
congenital dilation of dermal capillaries

Management
no treatment required
Dl2 Denoatology
Acneiform Eruptions
Toronto Notes 2011
Acneiform Eruptions
Acne Vulgaris/Common Acne
Clinical Presentation a common inflammatory pilosebaceous disease categorized with respect to severity Type I - comedonal, sparse, no scarring Type II - comedonal. papular, moderate :t: little scarring Type III - comedonal, papular, and p10tular, with scarring Type IV - nodulocyatic acne, risk of severe scarring predilection sites: face, neck, upper chest, and back Pathogenesis o follicular hyperkeratinization blocks the secretion of sebum (comedones) o androgens stimulate sebaceous glands to produce sebum o anaerobic diphtheroid Propionibacterium acnes bacteria contains lipase, which converts sebum to free fatty acids and produces pro-inflammatory mediators
Type II - Papular
Type I - Com1donal
Epidemiology age of onset in puberty (10-17 years in females, 14-19 years in males) more severe in males than in females incidence decreases in adulthood genetic predisposition: majority of individuals with cystic acne have parent(s) with history of severe acne Differential Diagnosis o folliculitis, keratosis pilaris (upper arms, face. thighs), perioral dermatitis, rosacea
Type Ill - Pustular
Management o see Table 8

Table B. Acne Treatments and Mechanisms of Action
Drug Name MILD ACNE: Topical Therapies Mechanism of Adi111 Lincosamide antibiotic; mibib; protuin synthesis Macrolide antibiotic; inhibits protein synthesis Prolain oxidant bactericidal &Ifact
dindmycil [e.g. Dllacin
Generally regarded as un&afu in lactation Local skin reactions include bumin{l peeling, dryness, erythema Dry skin, contact dennalilis Apply to the point of ctyness and erytluma, but not discomfort See above
Type IV- Nodulocptic

C Shelley Olen & Klislino Neuman, 2010
erytlnmycin benzoyl p.-oxide
Figure 3. Types of Acne
....
, ,.----------------.
BenzaCiin gel
1% clindamycin and 5% benzoyl peroxide
+ benzoyl peroxide [Bemamyci1.,

ldapal11111 [a.g. lliffllrin"l
lnlliaain [a.g.
3% etVihromycin and 5% benzoyl peroxide See above Comadolytic Comedolytic
Acna Myt... Dellunklld
Eating greasy food and chocolate does not CIIUII8 or WQIQIIICne Blackhllda (comldones)al'l black because of oxidimd melanin. not dirt
Lass irrilllting thenlrlltiloin. No intnction with sun

Sun sensitivity and irritation
llltin-A8
MODERA1E ACNE: Aftar topical treatments hiiVB failed, add oral antibiotics, such as tstracycline {500 rng PO daily to bid), or erythromycin [500 mg PO bid). Antibiotics require months of use before assessing ellicacy. Consider honnonaltherapy, includilg antiantt"ogens tllnlcycline Systemic antibiotic Cyproterone: potent anti-androgenic, progestogenic and antigonedatmphic activity Use caution with ll!{lard to drug interactions: do not use isobetinoin After 35 years of age, estrogerv'progesterane should ort{ be considered in exceptional circumstences, cal'tlfully wBighilg the risk/benefit ratio with physician guidn:e
....
,}----------------.
.A.. Exacertladng flelllrs

Systemic medications: lithium, phenytoi1, steroids, halog..,., ll!drogens, iodides, bnJmides, daiiiZol Topicllavem: mroida, !ani, ointments, oily cosmatics Mechanical prenure or occlusion, such II leaning fac1 on hand& Emational slnla
c:ypratBroae al:llatMthi estradial [Dilllll-35.,
Ethinyl Bltnldal: inc11111sas IIIVBI of SilK

hannane bilKing globulin [SHBG), reducing circulating plasma levels of antt"ogens
Toronto Notes 2011
Acneiform Eruptiona
Dermatology D13
Tabla 8. Acne Traatmants and Mechanisms of Action Icontinued)
Dnlg Nama Mechanilm of Adi111 Nllllll SEVERE ACNE: Consider systemic retinoids after above 1realments have failed Retinoid that inhilils sebaceous function and regluates keratinization Teratoganic: contraindicated during pregnancy,
unsale in lactation; reliable contraception is necess!rf
....._._______________ ,
IIOhlinoin and Lipids r.ports indicabl isDirltinoin-
Signed informed co115811t is needed when pllllicribing Baseline lpid profile, hepatic enzymes and before treatment May transiently exacerbate acne May cause depnession Drug may ba discontinued at 1620 weeks whan nodule count has !hipped by >711% A second course may be initiated r 2months pm Refractory cases may require 3 or more courses of isotretiloin
inducad hypurtriglycaridsmia can be succnsfully controlled with concurrent hypolipidernic therapy.
ea..
Perioral Dermatitis
Clinical Presentation discrete erythematous micropapules that often become c:ontluent, forming inflammatory plaques on perioral and periorbital skin c:ommonly symmetrkal, rim of sparing around vermilion border of lips aggravated by topical glucocorticoids Epidemiology 15-40 years old predominantly females Differential Diagnosis dermatitis, rosacea. acne vulgaris Management topkal: metronidazole 0.7596 gel or 0.75-1')6 cream to area BID systemic: tetracycline
Rosacea
Clinical Presentation chronic: acneiform, inflammatory skin disease flushing (transient erythema) with a burning sensation is common initially, however nontransient erythema is the c:ommonest sign of rosac:ea dome-shaped red papules pustules, contributing to a florid. ruddy complexion differentiated from acne by the absenc:e of c:omedones sites typically affected: convexities of the central face (forehead. nose, cheeks and chin) may also affect the scalp, neck, and the upper part ofbody characterized by remissions and exac:erbations all forms of rosacea can progress from mild to moderate to severe in longstanding rosacea. signs of thickening, induration, lymphedema in the skin phyma: a distinct swelling caused by lymphedema and hypertrophy of subcutaneous tissue, particularly affecting the nose (rhinophyma) ocular manifestacions: conjunctivitis, keratitis, iritis exacerbating factors: heat, cold. wind. sun, stress, drinking hot liquids, alcohol, caffeine, spices (triggers of vasodilatation) Pathophysiology
unknown
....._._______________ ,
Guidll&nN fw IIIII Diagnasis of lloACIIII Presence af ana or mare af 1he folowing primary features:
Flulhing (transient erythema)
Tallngiactasil
Nontl'll1sient erythema Papulus and puldul811
May includu onu or mare af the fallowing secondary features: Burning or slingilg
Dry lpjlllllr&rlCB
Edema Phymatous ch11111es Ocular m1111ifa!Biions Periphelllllocation
Epidemiology although found in all skin types, highest prevalence in fair-skinned people 30-50 years old
F>M
D14 Denoatology
Acneiform Erupti0ll8/Dermatitis (Eczema) Management
Toronto Notes 2011
......
t-----------------,
Sulltypelnd V.ri....
Their CMraeblrimicll
of._..
nd
SUIITYPE
Flushing, persistmt central facial erytlleiTIII 1BIIIIIUiec:tnia
Papulopustular l'lnistent central facial erythema

Transient central facial papul11 or pustules or batl1
Phyml&oul
avoid topical corticosteroids cosmetic camouflage telangiectasia: treated by physical abation; electrical hyfrecators, vascular lasers, and intense pulsed light therapies phymas: treated by physical ablation or removal; paring, electrosurgery, cryotherapy, laser therapy [C02, argon, neodymium-doped yttrium aluminum garnet (Nd:YAG}] early diagnosis and prompt treatment are recommended to prevent worsening
T1ble 9. Specific RoS1ce1Treatments

!It line
Znd Line
3nl Line
Thickening skin, inegulllr surface nodularitiN and enlarvement Nose, chin, forehesd, cheeks or eers
Oral tetracyclines mg PO bid) Topical mutronidazcle Oral erytlrurnycin (250-500 mg PO bid)
Topical clildarnycin Topical eryllromycin 2% solution Topical benzoyl peroxide

Dnll metrunidamle
Oral retinoids Topicaldw"
Ocul8r Fnign body Mnsation in the eye,

burning or lllinging, dryness, itx:hing, DaJiar blumd vision, tlllangiec1ll5il. of the sclera or other parts of thleye, or periorMal edema
Ampicillin
Dermatitis (Eczema)
Definition
inflammation ofthe skin
VAliANT Gr.nulclnl8tiM
uniform size
Noninflammatory, hard. brown, yellow, or rad cutaneous papula or nodul11 of
symptoms include pruritus and pain acute dermatitis: papules, vesicles subacute dermatitis: scaling, crusting chronic dermatitis: lichenification, xerosis, fissuring
Asteatotic Dermatitis
diffuse, mild pruritic dermatitis secondary to dry skin very conunon in elderly, especially in the winter (a.k.a. "winter itclt") but starts in the fall
Management
skin rehydration with moisturizing routine
mild corticosteroid creams
Atopic Dermatitis
--------------------------------------
......
, ...-----------------,
subacute and chronic eczematous reaction associated with prolonged severe pruritus distribution infant (onset at 2-6 months old): face, scalp, extensor surfaces childhood (>18 months): flexural surfaces adult: hands, feet, flexures, wrists, face, forehead, eyelids, neck inflammation, lichenification, excoriations are secondary to relentless scratching atopic palms: prominent palmar creases associated with keratosis pilaris (hyperkeratosis ofhair follicles, "chicken skin") xerosis occupational hand dryness
Trigers t.r Atopic: DIPIIIIItitia lrrimnb (dnrgentl, sol,.nts, Contact allarg &lvironmentalaeroall1r91ns (dust miiN) IIIIJiproprilrte bathing habits (long hot showers) SWe8ting
clothing, water hlrd111111)
Microbes (S. - . ) Strus
Epidemiology
frequently affects infants, children, and young adults females only slightly more at risk than males ( 1.3:1 over the age of 2 years) almost 15% of children in developed countries under the age of 5 are affected; half of these cases are diagnosed by 1 year of age associated with personal or family history of atopy (asthma, hay fever, anaphylaxis, eosinophilia) polygenic inheritance: one parent >60% chance for child; two parents >80% chance for child childhood onset and hereditary forms may be associated with a defect in the protein filaggrin the earlier the onset. the more severe and persistent the disease long-term condition with 1/3 of patients continuing to show signs of AD into adulthood
Pathophysiology
Th2 cellular response
Investigations
no gold standard for diagnosis consider: skin biopsy, immunoglobulin serum levels (often elevated serum IgE level), patch testing, and skin prick tests
Toronto Notes 2011
Dermatitis (Eczema)
Dermatology DIS
Management goal: reduce signs and symptoms, prevent or reduce recurrences/flares better outcome (e.g. less flare-ups, modified course of disease) if diagnosis made early and treatment plan individualized individualized based on age, severity, sites and extent of involvement, presence of infection, previous responses to therapy avoid triggers of AD enhance barrier function of the skin regular application of moisturizers emollients hydrate the skin and reduce pruritus twice daily application is recommended even in absence of symptoms, especially after bathing or swimming bathing promotes hydration when followed by the application of moisturizers to the skin anti-in11ammatory therapies A. topical corticosteroids effective, rapid symptomatic relief of acute flares best applied immediately after bathing control inflammation with a potent topical steroid; a milder one following resolution of acute flare systemic immunosuppression may be needed in severe cases flares may respond to systemic anti-staphylococcal therapy side effects: skin atrophy, purpura, striae, steroid acne, perioral dermatitis, and glaucoma when used around the eyes B. topical immunomodulators long-term management calcineurin inhibitors include pimecrolimus (Elide!), tacrolimus (Protopic) side effects: skin burning, transient irritation advantages of immunomodulators over long-term corticosteroid use rapid, sustained effect in controlling pruritus no skin atrophy safe for the face and neck Complications infections treatment of infections topical mupirocin or fusidic acid oral antibiotics (e.g. cloxacillin, cephalexin) for widespread S. aureus infections
lnililll amant af d i - hiltllry, extant and unrity (impact an fami!r, ..
I
Adj1nc:tiva th. .py Avoidance of triggers T11111t bacterial superinfections (topical or oral antibiotics) Antihistaminas Psychological interventions
"-tiant aducaliun, daily amullillllt uu
Ac... af flare Topical corticosteroids or topical calcinaurin inhibitor (pimacrolinus or111crolimus)
dlllrwa)
I
Dileala ramilliun (na signs symptams)
Mailtan..- tharapy is ..rsist.nt an.Vor fraqnt I'KIII'I'IIncas Use of topical corticosteroid or calcineurin inhibitor at sign offlara
long-term maintenance use of calcineurin inhibitors
Strvara rafractury dilaua Azathioprine Phototherapy Mlllhotraxate Potent topical steroids 01'11 cyclosporin P-vchotherapeutics 01'11 steroids
Figure 4. Atopic Dannltitis Treatment Algorithm

Adljad from: Blis C, at II.ICCAD II Faly.lntlmational Con1111sus Conferanca on Alopic Dermatitis II (ICCAD II): cilical updata and amntv.tmant ilmlagin.BrJilllmrltui.ZOOJ;
Dl6 Denoatology
Dermatitis (Eczema)
Toronto Notes 2011
Contact Dermatitis
Top T111 Allllrgen ldntililld by The
North Ameri01n Cont.ct Dennatitis Group
Clinical Presentation cutaneous inflammation from the interaction between external agent(s) and the skin
Tabla 11. Contact Dannatitis
Irritant Contact Dematitis
All-aic Contact Demllitis

Cel-mediated delayed {Type IV)
reaction Erythema with a pruritu& eruption, swelling.
Mechanis11 al Reaction
NckBI1.11f111 14.2 Found i11111111 Mllstclllm1'l)dyull8d
FrlgrlllC8 rratnl
Toxic injury to skin; nan-inmune mechalism Erythema, dryness. fine scale, burning .Acut8: quick reaction, &harp margins {e.g. from ecidfalkali expDSUrel Cumulative insult: slow to appear, poar1y defined margins (e.g. from sDapl. more common Majority; will occur in lllYOile given sufficient concentration of irritants Palmll' surface crf hand usually involved
Naon'rjcinsuhtl 13.1
Type al Reactian
fDiical anlibiric
llll11m of Fvru
11.8 11.7
Fnvance mix
Amix of e9rt dllarantfrlplce t:OITlponantl whicll -dMioped tDIIkrNiorallelgen tilting in COIIIIItics

ACGIIIIIDII ]JIISliYitivethdis
l:lllll'illlics
Frequancyal Canlllc:l Dannatitis
Minority; patient acquires susceptibility to allergen that parsists ildafinataly Dorsum crf hand usually involved; oftl!n discrete area of skin involvement
Diltributian
Exanlplll
Thi11111U1al
10.9
used in vaccilas, solution.
Soaps. weak alkali, detergents. organic solvents, (See sidebar! alcohol, oils Many allergens are irritants, so may coincide with irritant dermatitis Avoidance of irritants Wat compresses with Burow's solution Barrier moisturizers TopicaVoral steroids
Manqement
Sodium gold
lllldinjBWIIilry, delllistJy. thiosullltB elllCtn!Mcs
Patch blsting to dtJialmile specific allergen Avoid allergen 111d ib cross-reactants Wet COIJ1lresses soaked in Burow's solution
(drying agent)
9.3
Acobntess gu
found illl'lllll' wartpi!CII, l:lllll'illlics.
Steroid cream ihydrocortisone 1%. b81lm81hasane valllllla 0.05% or 0.1% cream; bidl Systemic steroids pm (prednisone 1mg/kg. taper owr2weeksl
11*1ic8tions. flldilas, resins,plasticbGitles

ILnmiurn-15
9.0
Dyshidrotic Dermatitis
Clinical Presentation "tapioca pudding" papulovesicular dermatitis of hands and feet that coalesce into plaques, followed by painful fissuring acute stage often very pruritic secondary infection common lesions heal with desquamation and may lead to chronic lichenification sites: palms and soles dorsal surfaces ofhands and feet Pathophysiology NOT caused by hyperhidrosis (excessive sweating) emotional stress may precipitate the dermatitis Management topical: high potency corticosteroid with plastic cling wrap occlusion to increase penetration intralesional triamcinolone systemic: prednisone in severe cases antibiotics for secondary S. aureus infection
11'1111\'lhllmpoos,
mcilflllm,.
Cobak clmla
9.0
aJI'Iditianen 11111 lOIIlS Al'llldmetalfound in
linin. tDals
Blcitlllcil
8.7
AfDpic:allllfibiatic
Nummular Dermatitis
Clinical Presentation annular, coin-shaped, pruritic, erythematous plaques, dry, scaly, lichenified often associated with atopic and dyshidrotic dermatitis secondary infection common Management rnoisturization corticosteroid ointment BID
Toronto Notes 2011
Dermatitis (Eczema)
Dermatology D17
Seborrheic Dermatitis
Clinical Presentation greasy, erythematous, yellow, scaling papules and plaques in areas rich in sebaceous glands infants: one cause of"cradle cap
children: may be generalized with flexural and scalp involvement adults: diffuse involvement of scalp margin with yellow to white flakes, pruritus, and underlying erythema sites: scalp, eyebrows, eyelashes, beard, glabella, post-auricular, over sternum, trunk, body folds, genitalia
Pathophysiology possible etiologic association with Pityrosporum ovale (yeast) Epidemiology common in infants and at puberty increased incidence in immunocompromised patients (e.g. HIV) in adults, can cause dandruff (pityriasis sicca) Management face: Nizoral cream OD +mild steroid cream ODor BID scalp: salicylic acid in olive oil or Derma-Smoothe FSlotion (peanut oil, mineral oil, fluocinolone acetonide O.ol %) to remove dense scales, 2% ketoconazole shampoo (Nizoral), ciclopirox (Stieprox) shampoo, selenium sulfide (e.g. Selsun) or zinc pyrithione (e.g. Head and Shoulders) shampoo, steroid lotion (e.g. betamethasone valerate 0.1% lotion bid)
Stasis Dermatitis
Clinical Presentation persistent skin inflammation ofthe lower legs with brown pigmentation, erythema, xerosis, and scaling associated with venous insufficiency Management support stockings rest and elevate legs moisturizer to treat xerosis mild topical corticosteroids to control inflammation Complications ulceration (common in medial malleolus), secondary bacterial infections
Lichen Simplex Chronicus

Clinical Presentation chronic dermatitis resulting from continued rubbing/scratching of skin may develop secondarily to another pruritic skin disease lichenified (thickened) skin Management treat pruritus to break the itch-scratch cycle: antihistamines, topical antipruritics topical corticosteroids (extremely potent)
DIS Denoatology
Papuloaquamous Diseases
Toronto Notes 2011
Papulosquamous Diseases
Lichen Planus
acute or chronic inflammation of mucous membranes or skin characterized by violaceous papules, especially on flexural surfaces small, polygonal, flat-topped, shiny, violet papules; resolves into hyperpigmented macules sites: wrists, ankles, muc:ous membranes in 60% (mouth, vulva, glans), nails, scalp Wickham's striae: greyish lines over surface; pathognomonic mucous membrane lesions: lacy, whitish reticular network. milky-white plaques/papules; increased risk of sec in erosions and ulcers nails: longitudinal ridging; dystrophic scalp: scarring alopecia spontaneously resolves in weeks or lasts fur years (mouth and shin lesions) Koebner phenomenon "isomorphic reaction": develops in areas oftrauma
The 6 P's uf Uch... PIPurple, Pruritic, Polygonal, Peripheral, Papules, Penis (i.e. lnjCOSil}
Epidemiology association with hepatitis C may be triggered by severe emotional stress Management
topical corticosteroids with occlusion or intradermal steroid injections short courses of oral prednisone (rarely) photochemotherapy for generalized or resistant cases oral retinoids fur erosive lichen planus in mouth
Pityriasis Hosea
acute, self-limiting, erythematous eruption characterized by red, oval plaques/patches with central scales that do not extend to edge oflesion long axis oflesions follows parallel to ribs producing "Christmas treeD pattern on back varied degree of pruritus most start with a "Herald" patch which precedes other lesions by 1-2 weeks sites: trunk. proximal aspects of arms and legs
Etiology
suspected human herpes virus 7
Management
none required; clears spontaneously in 6-12 weeks, reassurance topical corticosteroids when post-inflammatory pigmentation is a concern
Psoriasis
It' PSORIASIS: "'-ntttion ond
Classification
1. plaque psoriasis 2. guttate psoriasis 3. erythrodermic psoriasis 4. pustular psoriasis 5. psoriatic arthritis
Pink
bleeding
(Auspitz signi/PI1ysical injury (Koebner phanomanon} Silver scale/Sharp mBrgins spots Rata Ridges with lagulsr elongation
atopic dermatitis, mycosis fungoides (cutaneous T-celllymphoma), seborrheic dermatitis, tinea
Itching
ArthritiiVAbscns (MunroVAu1Dimmun Slnltum corneum with nuclei Immunologic
Diagnosis
often clinical, biopsy to confirm PASI (Psoriasis Area and Severity Index) score is based on: percentage of surface area involved and the severity of symptoms (erythema, infiltration, desquamation)
Slnltum granulosum absent
Toronto Notes 2011
Papuloaquamous Diseases
Dermatology Dl9
1. PLAQUE PSORIASIS
Clinical Presentation chronic and recurrent disease characterized by well-circumscribed erythematous papules/ plaques with silvery-white scales worse in winter (lack of sun and humidity) Koebner phenomenon "isomorphic response": induction of new lesion by injury Auspitz sign: bleeds from minute points when scale is removed usually non-pruritic exacerbating factors: drugs (lithium, ethanol, chloroquine, beta-blockers), stress sites: scalp, extensor surfaces of elbows and knees, trunk, nails, pressure areas Pathophysiology decreased epidermal transit time from stratum basale to stratum corneum shortened cell cycle of psoriatic compared to normal skin TIU -mediated inflammatory response Management preventative measures avoid sunburns avoid drugs that exacerbate the condition (e.g. beta-blockers, lithium, corticosteroid rebound phenomenon, interferon} first-line treatment mainly topical, usually prescribed if less than 5-10% oftotal body surface area is involved first-line topical treatments include moderate to potent steroids, vitamin D analogues, retinoids, anthralin, coal tar, salicylic acid ifthe affected area is >10%, use topical medications as adjuncts to phototherapy or systemic drugs second-line treatment include cyclosporin, methotrexate, acitretin, phototherapy third-line treatment biologics including alefacept, etanercept, intliximab, adalimumab, ustekinumab systemic treatments should be considered if: psoriatic lesions cover >10% of total body surface area unsuccessful topical therapies psychological distress
....
't-----------------, ,
PSORIASIS: Triggers (Koebner'1 ph-menan)
lnfactions (acubl mptococcal infection

pracipitatu& guttate psoria1i1) Strass (can baa major factor in flares) Drugs (l'(slumic gmocorticoidl, and lilllium, antimlllarilll drugs, inmrferun) Alcohol ingestion
lofi:al T..-.afGrCinlic .... 1'11ri181

lllua 2
-
C<nne
2U09,
'lillniiD.
piiiiBI.
Sysllnri: IIWw alllncbnizld trills c:ampllil; tnmem IQiinst J8;ello ...
lnllnlnliln: CarlicGitiRidl. diltniJI,

corlicDIIIInlidl. Dlilllml: IIMI1igltDr a-.!aiiMIIII gbbll Talll-ny-SCIRS.I'Ior8sisaa
Wlmil D,llldmrril D+
1111d.wity illllll'l1ilnt.-lai1M1111
Ill*: Cri:llllaroidt, villnil and 1mluln peliDrmud bllbl'lllln piiM alona. A c:oriinltion at cri:OIIIsroids and villmil D Willi batllr 1hln litlmWinin D corlicoltaroils aloal. II'
Tabla , , . Topical Treatment of Psoriasis

Tnlltmlnt LWicaniB Salicylic acid 1-12%
Tar (LCD: Liquor carbonis detergans)
20% coal tar sokltion
Reduce fissure formation RemOVII seal lrllibits DNA synthesis, increases cal
tumDVI!I
Putrolatum is effectiw Poor long term compliance

Not ID be used on face or skin folds
Use appropriete potency steroid in difhmrt arees for degree of psoriasis Use on nais
....
Caldpotriol i8 a vlbunm Dd.W..tin

considerad 1o be !he most potent topical psoriatic therapy.
'.,
Calcipotriene
(Dovonax",
Binds to skin keretinocyte proliferation

1,25dihydroxyvitarrin DJ ID inhibit
with batamathasona diprupionata and is
calcipotriallll combined
Corticosteroid oinbnent
Reduce scaling end thickness Retinoid derivatiw
Tabla , 2. Systamic Tralltmant of Psorinis Tnlltmlnt Methotrexate Bone maiTIIW toxicity, hepatic cirrhosis Psoralens end long wave ultraviolet radiation (PINA) Pruritus. burning. cetaracts, skin cancer
Alopecia, cheilitis, teraiDganicity, apislaxis, xerosis, hyperlriglyeridamia
Cyclosporine
lNB and "Narrow band"INB (311312 nm)
Renal toxicity, hypertansion, immunosuppniSSion

Wall tolerated
Tabla , 3. Biologics approved in Canada Tnlltmlnt Routa Dulling Sc:hedull

etanarcept {Entnl)*
adalirrumab (Humira)*
Etfll:tinn. .
Action
sc sc
IV
Twice weBidy initially Once wery 2weeks -Every 2 months

Every 12 weeks during maintenance
+ +++
++++
Tcell
....
infliximab (Remicade)* ustekinumab (Stelara)
sc
+++++ ++++
TNF TNF TNF

IL 12/23
,,,
Mechanism of Blalogla "mab" - monoclonal antibody capt" = recaptor
'Can lim be us1D 11111 ]JI01il1ic 11111ritis
D20 Denoatology
Papulosquamous Diseases/Vesiculobullous Diaeases
Toronto Notes 2011
2. GUTTATE PSORIASIS (DROP-LIKE;

discrete, scattered salmon-pink scaling papules sites: generalized, sparing palms and soles often antecedent streptococcal pharyngitis
Management
UVB phototherapy, sunlight, lubricants penicillin V or erythromycin if Group A beta-hemolytic SITeptococcus on throat culture
3. ERYTHRODERMIC PSORIASIS
generalized erythema with fine desquamative scale on surface associated symptoms: arthralgia, severe pruritus may present in patient with previous mild plaque psoriasis aggravating factors: lithium, beta-blockers, NSAIDs, antimalarials, phototoxic reaction, infection
Management
hospitalization, bedrest, IV fluids, monitor fluid and electrolytes treat underlying aggravating condition, sun avoidance methotrexate, cyclosporine, UV, oral retinoids, biologics
4. PUSTULAR PSORIASIS
sudden onset of erythematous macules and papules which evolve rapidly into pustules, very painful can be generalized or localized to palms/soles patient usually has history of psoriasis; may occur with sudden withdrawal from steroid therapy
Management
methotrexate, oral retinoids, biologics
5. PSORIATIC ARTHRITIS
5 categories asymmetric oligoarthropathy distal interphalangeal (DIP) joint involvement (predominant) rheumatoid pattern (symmetric polyarthropathy) psoriatic arthritis mutilans (most severe form) predominant spondylitis or sacroiliitis see Rheumatology; RH21
Vesiculobullous Diseases
Bullous Pemphigoid
chronic autoimmune bullous eruption characterized by pruritic, tense, subepidermal bullae on an erythematous or normal skin base sites: flexor aspect of forearms, axillae, medial thighs, groin, abdomen, mouth (33%)
Pathophysiology
Pa11phlgus Vulauls vs. Bulous Pallphigoid
VUI(IBril intraapidarmal, flaccid lesions PemphigoiD. = D.eepar, tense lesions at the junction
IgG produced against dermal-epidermal basement membrane proteins (hemidesmosomes) leads to subepidermal bullae
Epidemiology 60-80 years old

associated with malignancy (rarely)
Investigations
immunofluorescence shows deposition of IgG and C3 in the basement membrane anti-basement membrane antibody (IgG) (pemphigoid antibody detectable in serum)
Prognosis
generalized bullous eruption heals without scarring rarely fatal
Toronto Notes 2011
Vesiculobullous Diseases
Dermatology D21
Management prednisone steroid-sparing agents (e.g. azathioprine) topical potent steroids (clobetasol) may be as effective as systemic steroids tetracycline nicotinamide is effective fur some cases dapsone for milder cases
Dermatitis Harpetiformis
-------------------------------
Clinical Presentation grouped papules/vesicles/urticarial wheals on an erythematous base. associated with intense pruritus, burning. stinging almost always excoriated, rarely seen as blisters lesions grouped, bilaterally symmetrical sites: extensor surfaces of elbows/knees, sacrum, buttocks, scalp Pathophysiology 90% have HLA B8, DRJ, DQWZ 90% associated with gluten-sensitive enteropathy (celiac) (80% are asymptomatic) 30% have thyroid disease; some have intestinal lymphoma or iron/folate deficiency Epidemiology 20-60 years old, M:F = 2:1 Management dapsone fur pruritus gluten-free diet
Pemphigus Vulgaris
----------------------------------....
Clinical Presentation autoimmune blistering disease characterized by flaccid, non-pruritic epidermal bullae/vesicles on an erythematous or normal skin base may present with erosions and secondary bacterial infection sites: mouth (90%), scalp, face, chest, axillae. groin, umbilicus N"Ikolsky's sign: sliding or rubbing pressure on skin -+ separation of epidermis Asboe-Hansen sign: pressure applied to bulla causes it to extend laterally Pathophysiology IgG produced against epidermal desmoglein 1 and 3leads to intraepidermal bullae Epidemiology 40-60 years old, higher prevalence in Jewish, Mediterranean, Asian populations paraneoplastic pemphigus may be associated with thymoma, myasthenia gravis, malignancy, and use ofD-peni.cillamin.e Investigations immunofluorescence: shows IgG and C3 deposition intraepidermally circulating serum anti-desmoglein IgG antibodies Prognosis and Clinical Course begins with mouth lesions, followed by skin lesions first localized (6-12 months) then generalized lesions heal with hyperpigmentation but no scar may be fatal unless treated with immunosuppressive agents Management prednisone 1.0-3.0 mg/kg until no new blisters, then 1.0-1.5 mg/kg until clear, then taper steroid-sparing agents: azathioprine, methotrexate, gold, cyclophosphamide, cyclosporine, intravenous immunoglobulin (IVIG), mycophenolate mofetil plasmapheresis for acutely high antibody levels
,9.----------------. "
Pe..phig Foliac An autoimmune inlrlllpidermal blistaring disease that is more SL4!erficialthan pamphigus wlgaris due to antibodies against dasmoglain I, an intracellular adhesion molecule. Appears as crusted patchas and erosions which can initially be managed topical steroids if localizld. Activa widespread disease is treated like pemphi!Jls wlgaris.
....
,"
Azatllioprin1 Thiopurine malhyltnmsfanlse(TPMT] levels should be meBSUred before starting therapy. Individuals with low enzyme activity will axpariance graatar immunosuprassion.
D22 Denoatology
Vesiculobullous Diseases/Drug Eruptions Tabla 14. Summary of Vasiculobullous Disaasas

Bullous Psnpligaid Dannllitis H.-patifannis
lgA
Toronto Notes 2011
Psnphigus Vulgaris
lgG lnlriilepidermal
Eosinaphils 111d neutrophils
Altibady
lgG
Basement mentr.me
Eosinaphils
Dermal
Neutrophils
Gluten-free diet Dapsone
Systemic steroids lmmunosupn!SSive agents Tetracycline
High dose steroids Immunosuppressive agent (e.g. lmuran8 , mycophenolic acid) Malignancy with paraneoplastic
Clobstasol
Malignancy (rarely)
Gluten enteropathy Thyroid dis811S8 lntestinallymphD1118
Porphyria Cutanea Tarda

tense vesicles/bullae in photoexposed areas subjected to trauma facial hypertrichosis, brown hypennelanosis vesicles, and bullae in photo distribution (dorsum of hands and feet) sites: light-exposed areas subjected to trauma, dorsum of hands and feet. nose, and upper trunk
Pathophysiology
autosomal dominant or sporadic skin disorder associated with the presence of excess heme associated with alcohol abuse, DM, drugs (estrogen therapy, NSAIDs), mv, hepatitis C, increased iron indices
Epidemiology 30-40 years old, M> F Investigations urine+ 5% HCl shows orange-red fluorescence under Wood's lamp (UV rays)
24-hour urine for uroporphyrins (elevated) stool contains elevated coproporphyrins immunofluorescence shows IgE at dermal-epidermal junctions
Management
discontinue aggravating substances (alcohol, estrogen therapy) phlebotomy to decrease body iron load low dose hydroxychloroquine
Drug Eruptions
Drug Hypersensitivity Syndrome
Drug Hypena..ilivity Syndrame Trid
Exanthematous Eruption lntarnal 01'!1., lnvolvarnant
Fever
fever followed by symmetrical bright red exanthematous eruption that may lead to internal organ involvement (hepatitis, arthralgia, nephritis, pneumonitis, lymphadenopathy; and/or hematologic abnormalities) classically occurs approximately 10 days after first exposure to the drug siblings at risk most common causes: sulfonamides and anticonvulsants (phenytoin, phenobarbital, carbamazepine, lamotrigine) 10% mortality if undiagnosed and untreated
Erythema Multiform& (EM). Stevens-Johnson Syndrome (SJS). Toxic Epidermal Necrolysis (TEN)
disorders with varying presence of characteristic skin lesions, blistering and mucous membrane involvement NOTE: EM is considered to be distinct from the SJS-TEN spectrum
Toronto Notes 2011
Drug EruptiOJU
Dermatology D23
Table 15. Comparison ol Erythema Multilome, Stevens-Johnson Syndrome, Toxic Epidermal Necrolpis
E.ryt1111111
Multifanne (EMI
Stevens-Jallnson Synlhme (SJSI Toxic Epidennll NICI'IIIysis flfNI

EM with more mucous membrane invoiVI!IIII!nt "Atypical lesions": rad patch with dark purple centre "Sicker" {hilt! feverl Sheet-like epidennll detachment in < 10% {Nikolsky sign) Severe mucous membrane invoiVI!IIII!nt, and blistering "Atypical lesions": 50% have no target lesions Diffuse erythema then necrosis and sheet-like epidermal detachment in >30%
....
',
Lilian
Maculef/papules with central vesicles Classic bull's-eye pattern of concentric light and dart rings (target lesions) Bilateral and symmetric All lesions appear within 72 hours No edema Lesion "fixed" for at least 1 days
Erythmul multiform is 1 clinical diagno1i1. Resonabla evidence axim fur the following as precipitating factors: HSV (pqdomin1111t pl'8cipillllingfactorl
Myr;opluma ptlflllmonies
Orfviru&
scomrt As-ilt*._ San far Taxi:

Generalized with prominent face and 1nlnk involvement Palms and soles may be spared Generalized Nails may also shed
DoiSI of hands and forearms

Mucous membrane involvement (lips, 1D191e, buccal muCOSI) is possible Extremities with lace > 1nlnk lnvoiVI!IIII!nt af palms and soles Other Burning and stinging Complications Recurrences Secondary bacterial infection Constibdianal Weakn1155, malaise Symptom
Scarring, contractures, eruptive nevornelanocytic nevi, corneal scarring, blindness, phimosis and vaginal&ynechiae
Tubular necrosis and acute renal failure, epithelial erosions of trachea
Prodrome 114 days prior to High faver >38"C eruption with fever and ilness
Jbest Demllifri 2UMl;115:14S.153 S1udy: lleveio!l-.1 nlidllt updic QQrily af-il_s_lar CUll allEN and CDII1llftl 1D Simpllied AID l'lrjliolagy Score 1nd blln scaring &'jlllm. l'ltiiB To develp score IIIII evabite Diller .-.: 165 plli8IQ wi1b SJS.SJS/ItN, or TEN IIW1Id 1D the K:U. For Vllillliln,l sepnfl dltlbll8 gf 75 pltilnii\WII Ullld. llqi8CIIdand lCllll 11'l(ltJiy. rllill:rmr.tion. bulls: s-. diflrant risk fldln far dllth:
age>40y,lllllignlnl;y,lldlylrillbcM! 12D. illitiellpidennll dlllehmllll >I 11\, liMn Ural >10 mmoK,11m11 gtc >14 rrmol1.. ..t bicllil
Etiology
Infection: HSV. or Micoplasma pneumoniiJe
15% are drug-related (NSAIIls, anticorMJisants, sullcnamides, penicillins) Occurs up to 1-3 weeks alter drug exposure with more rapid onset upon rechallenge
50% are definitEly drug related <5% 1111 due to viral infection, immunization
<20 mmol'\. Expeclld . -QJI!tlllfed with IICUI 11'llltJiy (19.3 compnd fa 20'41; wlliiNS, 1he SAPS hid poor IIQ181111111111 llqlldBd ..t lttull molllily l9.1'lo VI.
Diflerentill Di111nD1i1
Giant urticaria, graooloma annulare, Scanet lever, photutoxic, eruption, Scanet lever, phototoxic eruption, myc08is fungoides, vasculitis gRift w. host disease {GVHDI. GVHD, SSSS, axluliative dermatitis staphylococcal scalded skin syndrome (SSSSI, exfoliative dermatitis, Kawasaki disease, paranaoplastic pemphigus Lesions last 2 weeks and heal without cDiflllications SyrqJIDmatic treatment {oral antihistamines, oral antacidsl Corticostaroids in severely ill (controwrsiall Prophylactic oral acyclovir for 6-12 months for herpes siiJ1llex virus (HSV)-associated EM with frequent recu1T811ces course 5% mortality Prolonged hospitalization Vllithdraw suspect drug htravenous fluids Corticostenoids (contiOV8nial) hfection prophytuis Consider IVIG
Coune;md
PragnDiia
Mulglllllllt
30% mortality due to fluid loss, regrowth of epidermis by 3 weeks, secondary infection
As for Stevens-Johnson syndrome Admit to bum unit Debride frankly necrotic tissue ConsiderMG
Exanthematous Eruptions (Maculopapular Eruptions/Morbilliform)

symmetrical, widespread, erythematous patches or plaques scales the "classic" and most common adverse drug reaction often starts on trunk or areas of sun exposure may progress to generalized exfoliative dermatitis especially if the drug is continued most common causes: penicillin > sulfonamides > phenytoin see Pediatric Exanthems, D40
Fixed Drug Eruption

sharply demarcated erythematous oval patches on the skin or mucous membranes sites: face, mucosa, genitalia reaccurs in same location upon subsequent exposure to the drug (fixed location) most common causes: antimicrobials (tetracycline, sulfonamides), anti-inflammatories, psychoactive agents (barbiturates), phenolphthalein
D24 Denoatology
Drug Eruptions/Heritable Disorders
Toronto Notes 2011
Photosensitivity Eruptions
phototoxic reaction: an exaggerated sunburn" confined to sun -exposed areas photoallergic reaction: an eczematous eruption that may spread to areas not exposed to light most common causes: chlorpromazine, doxycycline, thlazide diuretics, procainamide
Serum Sickness-Like Reaction

a symmetric drug eruption resulting in fever, arthralgia, lymphadenopathy, and skin rash usually appears 5-10 days after drug skin manifestations: usually urticaria; can be morbilliform most common causes: cefaclor in kids; buproprion (Zyban") in adults
Heritable Disorders
Ichthyosis Vulgaris
Clinical Presentation generalized hyperkeratosis leading to dry skin "fish-scale" appearance especially on extremities with sparing of flexural creases, palms and soles; scaling without inflammation Pathophysiology abnormal retention of hyperkeratosis scaling without inflammation Epidemiology 1:300 incidence autosomal dominant inheritance associated with atopic dermatitis and keratosis pilaris Management immersion in bath and oils emollient or humectant creams, and creams or oils containing urea
Neurofibromatosis
(Typal; von Rackllnghausans Disease)
Clinical Presentation diagnostic criteria includes 2 or more of the following: 1. more than 6 spots >1.5 em in an adult, and more than 5 spots >0.5 ern in a child under age 5 2. axillary or inguinal freckling 3. iris hamartomas (Lisch nodules) 4. optic gliomas 5. neurofibromas 6. distinctivebonykmon 7. first degree relative with neurofibromatosis type 1 associated with pheochromocytoma, astrocytoma, bilateral acoustic neuromas, bone cysts, scoliosis, precocious puberty, developmental delay, and renal artery stenosis Pathophysiology autosomal dominant disorder with excessive and abnormal proliferation of neural crest elements (Schwann cells, melanocytes) linked to absence of neurofibromin (a tumour suppressor gene) Epidemiology incidence 1:3,000 Management follow closely for malignancy, transformation of neurofibroma to neurofibrosarcoma excise suspicious or painful lemons see Pediatrics, P86
Toronto Notes 2011
Heritable Disordersllnfectiona
Dermatology 025
Vitiligo
primary pigmentary disorder characterized by hypopigmentation and depigmentation acquired destruction of mdanocytes characterized by sharply marginated white patches associated with streaks of depigmented hair, chorioretinitis sites: extensor surfaces and periorificial areas (mouth, eyes, anus, genitalia) Koebner phenomenon "isomorphic response": may be precipitated by trauma
IIIIMIIIilu fer \lilgo
Coclnlle Dl!rllase ofS)'st Rev 2010; Issue 1

S1udy: Sys1imllic nMiw rl1111damiltd controllll trills. l'atillll: 3139 pllticiplrltsNtllvitiiQO. lnlelwldion: TQI)ic:al treltmenl!, lghttheRpies, 01111
trallmlnll, _.1 mlllhods. Md

tt.lpias
Pathophysiology
acquired autoimmune destruction of melanocytes
ldverseella:ls
ReiIIIII: Modnta Mdancellldsls fa' 'die usa at

tupical carticosleloids111 incM:e H17NMt IIMna allacts II'B absarwd Ntll use. Topical use r1 nan-mroidal innrlmnlllillators (i.e. tacralu),ISpllcilly in
Epidemiology
1% incidence, polygenic 30% with positive family history
alriillltianNtlllighttlimpies, lllslllabaen
liiiMIIID ildue&l'llpi(Jnllnlltian.llawiM!r.IDnR1Brrn use Rlll'llillllticaltf incrasatlia risk lor cancer. In combirlllian thenpy incUdilg somafonn hlwJ 'dla mast improvemelf. Sustained rePtJnen1atia11 (>2 YtMI lu nat bean rapaT1Id nl tlu radsllhauld ba tra1111d with caution.
Investigations
rule out associated autoimmune diseases: thyroid disease, pernicious anemia, Addison's disease, TypeiDM Wood's lamp to detect lesions: iluminates UV light onto skin to detect patches of amelanosis
Management
sun avoidance and protection topical immunomodulator (i.e. tacrolimus, pimecrolimus) or a topical steroid for 6-12 months prior to attempting phototherapy PUVA camouflage preparations "bleaching" normal pigmented areas (Le. hydroquinone 20%) if widespread loss of pigmentation
M;/1 Oemrafti2007; 143: 578
.....
IIIMIIIizlllllauWHiind Trill rl Tnlllnat
S1ully: rllllbrized study. I'IIIIB 56 pililnll with nansagmlrllll Wilgo. IIIIMIIIilu: PINA or NS.lNB Mi:e per week
111rfaca areatliatwas
11111 cooornwlch COJiljlled111
attliund
Infections
Bacterial Infections
often involve the epidermis, dermis, hair follicles or periungual region systemic
SUPERFICIAL SKIN (EPIDERMAL)
IP<D.001 ). Alter48 -ions BSAmavwas Gre111er in the NB-IJIIB grrAip 11'=.007) dis benefit -mlirlllillldat12111DIIIIIs.
cithCRP'f, ni11112111C1111hs. ReiIIIII: NS.lNB il..,arior mPUYA.64\ ci 25 patients in the NS.lNB group sbled gleller tlwl m imp!DYIIIlllllt in BSA campllld 1D 36\ rl 25 pllicm1J in tha PINA!JOUP. Colu mlll:h WIS Qrelller in the NB-IJIIB grrAip 1hm the PUYA group
Tabla , &. Comparison of Impetigo Vulgaris and Bullouslmpatigo

Impetigo Vulpris
Clinical Pnentation
Bullmalmpetiga
Acute purulent infaction which app1111rs V8Sicular; Scattered, thil-walled bullae containing dear yellow progresses to golden yellow or slightly turbid fluid with no surrounding erythema lesions surrounded by erythema trunk, intertriginous areas, face Sites: commonly face, anns, legs and buttocks
Etiology
Epidllliolagy
S. aunws, or both
Group A beta-hemolytic Stn!ptococcus (GAS I,
S. 8llllliJS group II elabarating exfoliating toxin
Preschoolllld young allllts livilg in crowded Neonates and older chillhn, can be epidemic conditions, poor hygiene, neglected minor trauma Infected eczema, HSV, varicella virus Bullous drug eruption, perqngus wlgaris, bLJious insect bites, thermal bums Same as impetigo wlgaris Cloxacillin for 7-1 0 days Topical antibacterial5 such a5 fu5idic acid or mupirocin; continue for 7-10 days after 01111 antibiotic is CQI11llication: hill! levels of toxin in irrmmocompromised or young children may lead to genaralillld skin pealing or staphyloccocal scalded skin syndrome (SSSSI
lnndgations Mln11111ment
Gram stain and culture of lesion fluid or biopsy Remove crusts, use saline compresses and topical antiseptic &aalai bid Topical antibacterials such as 2% mupirocin or fusidic acid 110; continue lor 7-10 days after resolution Systamic antibiotics such as cloxacillin or caphalaxin for 7-1 D days
D26 Denoatology
Heritable Disonlenllnfections
Toronto Notes 2011
DEEPER SKIN (DERMAL)

Table17. Comparison of Erysipel11 and Cellulitis
Elysipells
Clilic:al Presanllltian Involves upper dennis Confluent, erythematous. raised, warm well demarutad Very painU (once called St. Anthony's fire) Sites: lace and legs Systemic symptoms: fever, chills, headache, weakness (if prunnt. siiJl of mora &erious infuction)
Cellulitis
Involves lower derrnil/subcubmeaus fat Unilatenll erythematous flat lesion, Dften vasicl111 poor1y dellllltiiiBd. nDt Wliformy raised Tender Sites: commort( on legs Sysll!mic symptoms (Wlcornnon): fever, leukDcytosis, lyrrflhadenopathy
Etiology
Compli.:n-
GAS
Scar181 fever, ilnlptococcaiiJillgrune, 1at necrosis, coaguloplllhy Spreads via lymphatics
GAS, S. ameus (1.-ge sized wounds), H. Blfluenzae (p&riorbital), Pastsur&lle muJtocidl (doQI'cat billl)
Uncommon
Diffli...UI DiiiiRDiil
M (less red. less hat. smoother). superficial phlebitis, contact dennatitis, photosensitivity reaction. stasis dennatitis,
Same as erysipelas
IIIVBitiglliona
Same as erysipelas Clirical diagnosis: rarely do skin/blood culture If suspect necratimg do immsdiatu biopsy and frozen section, histopathology
1st line: panicillin, ciCXBcillin or cllfllmlin Znd lile: clindamycin or cephalexin If allergic to penicillin use erythromycin 1st line: cloxacillin or cehizclinlcephalaxin Znd line: erythromycin or clindamycin Chldren: ceflnxime If diabetes (folll infections): trimelhoprimsulfamethoxazole (lMP/SMX) and mlllronidazole
COMMON HAIR FOLLICLE INFECTIONS

Table 11. Comparison of Superficial Folliculitis, Furuncl11 and Carbuncles
Superficial Folkulitis
Clinical Preselltltion
Superficial infection of the hair follicle (wraus pseudofolliculitis: inllammlllion of follicle due 1D friction, irritation, or occlusion) Al:utelesion consists of a dome-shaped pustule Ill the mouth of hair follicle Pustule ruptures 1D form asmal crust Sites: primarily scalp, shoulders, arterior chest. upper back, other hairbearing !1"8118 Normal non-pathogenic bact&ria [Stuphytococcus - most common;
Furunc:la (Boila)
Red, hot. tender, inflnmatory nodules central 'f'llllowish point. which forms over summit and ruptures Involves subcutaneous tissue that arises from ahair follicle Sites: heir-bearing skin (thigh, neck. face, axillae. perineum. buttocks)
C..rbuncllll
Deep-saatud abscess formed by coalescing luruncles Usually in areas of thicker skin Occasionally ulcerates L111ions chin through multiple openings to the surfece Systemic symptoms may be associated
Etiology
Pseudanool3- hot tub)

Pityrosporom
M-g-11: Antiseptic Topicalllltibacterial (lusidic ecid. mupirocin, or erytiYornycin) Oral ciCXBcillin for 71 0 days Incise and dran large carbuncles to Same as for luruncles relieve pressure and pain Hafebrile: hot wet pack.s, topical antibiotic Hfebrll1/celulitis: culture blood and aspirate pustules (Gram stain and C&S) Cloxaciln for 1-2 weeks (especially for lesions near BXtemal auditory canal/ nose, with suiTOWiding cellulitis, and nDt responsive to topical therapy)
Dermatophytoses
Clinical Presentation infection of skin, hair and nails caused by dermatophytes (fungi that live within the epidermal keratin and do not penetrate deeper structures)
Pathophysiology digestion of keratin by dermatophytes results in scaly skin, broken hairs, crumbling nails Etiology
Trichophyton, Microsporum, Epidermophyton species (Pityrosporum is a superficial yeast)
Toronto Notes 2011
Infections
Dermatology D27
Investigations skin scrapings, hair, and/or nail clippings analyzed with potassium hydroxide (KOH) prep to
look fur hyphae and mycelia
Management
topicals as first line agents for tinea corporis/cruris and tinea pedis (interdigital type): e.g. clotrimazole or terbin.afine cream applied OD or BID, until one week after complete resolution oflesions oral therapy is indicated for onychomycosis or tinea capitis: e.g. terbinafine (Lamisil -liver toxicity; CYP 206 inhibitor) or itraconazole (Sporanox heart failure reported, CYP 3A4 inhibitor)
Tabla , 9. Diffarant Manir.statiDnl af DarmatDphyta lnfaetiDn

Clnic:al Praentlltilln TinA Ci!pitis
Diflnntial Diagnolil
Inlitigations Wood's light axarrination of hair. IJ!I!n llucrescence ort, for Micmsporum infl!ction Cullure Ill scaie&tlai' shaft MiC105CDpic IIXilllination of KOH preparation of scales or hair shafts
M1111g11111nt Griseofulvin x 8weeks or terbi!Bina (Lamisil 411 2-4 weeks x NB: oral agents are required to penetrate 1he hair root Adjunctiw antifungal shampoos or lotions may be helpful {e.g. selenium sulfide, ketllconOZDie, ciclopilllX)
Round, scaly petchBI Ill alopecia, Alopecia al'lllllll, psoriasis, possibly broken Dfl hain; pruritic seborrheic dermatitis. Sites: scalp, eyelashes, and eyebrows; 1richotillomania involving hair shafts and follicles Kerion {boggy, elevated. purulent inflamed nodui!Vplaquel may form secondary to infection by bacteria and result in scarring May hiMI occipilllllymphadanopathy Affects children (mainly black). inmmocompromised adult! 'Wf contagious and may be transmitted from barber, hats, theatre seats, pet& Pruritic, scaly, round/oval pi8Cf.!e with Granuloma annulzn, pityriasis actiw erythematous margin and cantral rosaa. psoriasis, seborrheic clearing dermatitis Site: trurt, limbs, face Scaly patc!Vplaque with a curved border and central clearing Pruritic, arylhematnus, dry/macaratad medialthigh Pruritic scaling and/or macaration of the web spaces and powdery scaling of soles Acute infection: inlllrdigillll (esp. 4th web spacal rvd/white &ealas, wsicles. bulae. often d maceration Secondary bacterial i'lection is common Clmic: non-pnritic, pink. scalilg laraiDsis on soles aoo sides of feet May present as lin-up of chronic tinea pedis Pllldi5p0sing factors: heat. occlusive footwell' Candidiasis (involvement of scrotum and satale lesionsI. contact dermatitis, arylhrasma
Tin Corporis (RilgwDnnl
Microscopic examinations of KOH prep of scales shows hyphaa Culture of scales Same as for tinea corporis
Topicals: 1% clotrimazole or 2% miconamla BID for 2-4 waaks
Tin Cruris ("Jock ltch1
Topicals: 1% ciDirimazole or 2% miconamle BID for 2-4 weeks
TinR Pldis
(Atllletl's FDGI)
Atopic darrnatitis, contact Sarna as for tinaa corporis dermatitis. dyshidrotic dermatitis. erythrasma, intl!rbigo (interdigital), psoriasis
Topicals: 1% ciDtrimazola or 2% miconamle BID for 2-4 weeks
Manuwn
Primary fungal infection of the hand is Atopic darrnatitis, contact rare; usually associa1ed with tinea pedis dermatitis, granuloma annulare, Acute: blisbn at edge of red arBBI on psoriasis hands Clmic: single dry scaly patch Crumbling. dirtally dystrophic nails; yallowish, opaque with subW'CjuBI hyperkeratotic debris Toenail infections usually precede fingernail infections T.lllbrum (90% of 1111 to-il irnctionsl Psoriasis, lichen planus, contact dermatitis, 1nlumstic onychodystrnphies, bacterial infections
Sarna as for tinaa corporis
Topicals: 1% ciDirimazola or 2% miconamle BID for 2-4 weeks
Tinea un.,.ium (Cinyc.omycolill
Microscopic examinations of KOH prep of scales from subungual scraping shows hyphae Culture of subungual scraping or nail clippings on Sabouraud's agar
Tarbinalina (lmlisil 41) (6 waaks for fingernails. 12 waaks for to-is) ltraconazole (Sporanox) 7 days on, 3 weeks Dfl (2 pulses for fingernails, 3 pulses for toenails) Topical: ciclopilllX (Penlac411; naillaquar
Parasitic Infections
SCABIES
a transmissible parasitic skin infection due to Sarcoptes scabiei, a mite, characterized by superficial burrows, intense pruritus (especially nocturnal), and secondary infection primary lesion: superficial linear burrows secondary lesion: small urticarial crusted papules, eczematous plaques, excoriations sites: axillae, groin, buttocks, hands/feet (especially web spaces), sparing of head and neck (except in infants)
D28 Denoatology
Infections
Toronto Notes 2011
Pathogenesis scabies mite remains alive 2-3 days on clothing/sheets incubation of 1 month, then pruritus begins re-infection followed by hypersensitivity in 24 hours Etiology
Sarcoptes scabiei, a mite

risk factors: sexual promiscuity, crowding, poverty, nosocomial, immunocompromised
Differential Diagnosis asteatotic eczema, dermatitis herpetiformis (vesicles, urticaria, eosinophilia, no burrows), lichen simplex chronicus (neurodermatitis) Investigations microscopic examination of root and content of burrow with KOH fur mite, eggs, feces Management bathe, then apply permethrin 5% cream (i.e. from neck down to soles of feet (must be left on fur 8-14 hours and requires second treatment 7 days after first treatment) o change underwear and linens; wash with detergent in hot water cycle then machine dry o antihistamine o treat family and contacts o pruritus may persist fur 2-3 weeks due to prolonged hypersensitivity reaction LICE (PEDICULOSIS) Clinical Presentation o intensely pruritic red excoriations, morbilliform rash, caused by louse (a parasite) o scalp lice: nits (Le.louse eggs) on hairs red excoriated skin with secondary bacterial infection, lymphadenopathy o pubic lice: nits on hairs excoriations o body lice: nits and lice in seams of clothing excoriations and secondary infection mainly on shoulders, belt-line and buttocks Differential Diagnosis o bacterial infection of scalp, seborrheic dermatitis Management o permethrin 1% cream rinse) (ovicidal) or permethrin 1% (RC & Cor-, Kwellada-pe shampoo) comb hair with fine-toothed comb using dilute vinegar solution to remove nits repeat in 7 days after first treatment change clothing and linens; wash with detergent in hot water cycle then machine dry
Viral Infections
HERPES SIMPLEX
Clinical Presentation herpetiform (Le. grouped) vesicles on an erythematous base on skin or mucous membranes transmitted via contact with erupted vesicles or via asymptomatic viral shedding
primary
children and young adults usually asymptomatic; may have high fever, regional lymphadenopathy, malaise followed by antibody formation and latency of virus in nerve root ganglion
secondary
recurrent form seen in adults; much more common than primary prodrome: tingling, pruritus, pain triggers for recurrence: fever, sunburn, physical trauma, menstruation, emotional stress, upper respiratory tract infection (URTI) potential complications dendritic corneal ulcer erythema multiforme (EM) herpes simplex encephalitis HSV infection on atopic dermatitis causing Kaposi's varicelliform eruption (eczema herpeticum) 2 biologically and immunologically different subtypes: HSV-1 and HSV-2
Toronto Notes 2011
Infections
Dermatology D29
HSV-1 typically "cold sores" (grouped vesicles at the mucocutaneous junction which quickly burst) recurrent on face, lips but NOT on mucous membranes (unlike aphthous ulcers)
Management
...
Bllth HSV-1 and HS\1-2 can DCCII' on
fllce or genitalia.
treat during prodrome to prevent vesicle formation topical antiviral (Zovirax) cream, apply 5-6x/day,4-7 days forfacial/genitallesions oral antivirals are far more effective and have an easier dosing schedule
HSV-2 sexually transmitted; incubation 2-20 days gingivostomatitis: entire buccal mucosa involved with erythema and edema of gingiva vulvovaginitis: edematous, erythematous, extremely tender, profuse vaginal discharge urethritis: watery discharge in males recurrent on vulva, vagina, penis for 5-7 days diagnosis negative darldield. negative serology for syphilis, negative bacterial cultures Tzanck smear with Giemsa stain shows multinucleated giant epithelial cells tissue culture and electron microscopy of vesicular fluid skin biopsy antibody titres increase one week after primary infection only (no increase with recurrent lesions) DDx of genital ulcers: Ccmdida balanitis, chancroid. multiple syphilitic chancres
Management
rupture vesicle with sterile needle wet dressing with aluminum subacetate solution, Burow's compression, or betadine solution 1st episode: acyclovir 200 mg PO 5times a dayx 10 days maintenance: acyclovir 400 m.g PO BID famciclovir and valacyclovir may be substituted and have better enteric absorption in case ofherpes genitalis, look for and treat any other sexually-transmitted infections
HERPES ZOSTER (SHINGLES)

unilateral dermatomal eruption occurring 3-5 days after pain and paresthesia of that dermatome vesicles, bullae, and pustules on an erythematous, edematous base lesions may become eroded/ulcerated and last days - weeks pain is pre-herpetic, synchronous with rash, or post-herpetic severe post-herpetic neuralgia often occurs in elderly Hutchinson's sign: involvement of tip of nose suggests eye involvement distribution: thoracic (50%), trigeminal (10-20%), cervical (10-20%); disseminated in HIV
... , ,
Herpes Zoster typically involves a single darmatoma; lesions randy Cf1lll the midline.
Etiology
caused by varicella zoster in a person who has already had the primary infection (chicken pox) risk factors: immunosuppression, old age. occasionally associated with hematologic malignancy
Differential Diagnosis before thoracic skin lesions occur, must consider other causes of chest pain
contact dermatitis, localized bacterial infection, zosteriform herpes simplex virus (more pathogenic for the eyes than varicella zoster)
Management
compress with normal saline, burrow's, or betadine solution analgesics (NSAIDs, amitriptyline) for patients over 50 years old. with severe acute pain or ophthalmic involvement: famciclovir or valacyclovir for 7 days or acyclovir for 7 days ifimmunocompromised; must initiate within 72 hours to be ofbenefit gabapentin 300-600 mg PO TID for post-herpetic neuralgia
D30 Denoatology
Infections
Toronto Notes 2011
MOLLUSCUM CONTAGIOSUM Clinical Presentation
discrete dome-shaped and umbilicated pearly, white papules caused by DNA pox virus (Molluscum contagiosum virus (MCV)) sites: eyelids, beard (likely spread by shaving), neck, axillae, trunk. perineum. buttocks
Etiology
Molluscum contagiosum is spread via direct contact, auto-inoculation, sexual contact

common in children and AIDS patients
Management topical cantharidin (a keratolytic) liquid nitrogen cryotherapy curettage Aldara (imiquimod): immune modulator that produces a cytokine inflammation WARTS (VERRUCA VULGARIS) (HUMAN PAPILLOMA VIRUS (HPV) INFECTIONS) Table 28. Different Manifestations ol HPV Infection
lleliniliDn and Cli1icll Fllllures
lliffaranlill
Molluscum contagiosum. sebollheic keratosis
Venue: Vulgaris
(Common Wlrtl)
Hyperkeratotic. elevated discrete epithelial growths with papilill8d surface caused by HPV - at least 80 types 818 known Located at1nluma sites: fingn, hands, knees of c:hillhn and teens Paring of surface reveals punctill8, red-brown spscks {dili118d capilaries) Hyperbratatic. &hiny, sharply rnarginill8d growtiJ& HPV 1,2, 4, 1D Located at pressure sites: heads of mellllarsal, heels. toes Paring of surface reveals r&d-brown spscks (capileries). inllrruptian of epidermal ridges Muftiple discndB, skin colourad, flat topped papules grouped or in linear configuration Common in children HPV 3, 10 Sites: fees, dorsa of hands, shin&, knees
Venuc:a Pllllflris
(Plantar Wvll)
Need to scrape ("para") lesions to differentiate wart from callus end com {see side bar DB)
llld
Venue: Palmaris (Pal011r W..rta) Venuc:a PIIIIIG IFiiltWarta)
Syringoma, seborrheic keratosis, molluscum contagiosum. lichen planus
Candylama ACIIninata (Genilllll Wart.)
Skirt-coloured pmead papules to soft cauliflower Condyloma Iiiii! (secondary le&ion. darkfiald like masses i1 clusters strongly +vel, Molluscum contagiosum HPV 6 and 11 HPV 16, 18, 31, 33 cause cervical dysplasia. squamous call cancer and invasive cancer Sites: genitalia end parianaleraas Oftsn occurs in young adults, infants, children Can be asymptomatic, lasting months to years Highly contagious, tla\Siritled sexually and nor.sexually {e.g. Koebner phenomenon viii scratching. shavilg), end can spread without clinically apparent lesions Investigations: acetowhitening (subclinical lesions S81111 with 5% ecatic acid x 5 minutes and hand lens) Complications: fairy-ring werts {satellite warts at pl!f1lhery of treated area of original warts)
Toronto Notes 2011 Table 21. Management of Warts

Mln1111m111t
Dasbuc:livll Li(Jlid nitrogenfeleclrodesiccation Surgery
Infections
Dermatology D31
Type of Wart
All Resistant Resistant Small, CQI!lmon Cornnon Genital
Nates Dyschromia, pain, 11h!O seconds Scar, recurrence and Nd: Vag lasers Klnlolytic irritation, blistErs, hyperpigmentation Irritation, blisters, scar Erythema, erosions, ulcers, pain Pain, 111illo8Wdyslrophy, Reynaud' ph1111omanon CauSBI an Erythema, I'IIIICtion erosion
.....
'9t-----------------, '
r-tmllll tar Slcin wn
Fint Unllhlrpla
Salicylic acid preparations (patches, solutions, ointments] Silver nitnJte stick Topical c.rtharone
Laser
C.ullic Acids
Cantharidin (topical) Mono-, artri-chiOiliCelic acid Chemlllharapalllic Agants Podophyllotoxin*
Glutalaldet!yde
Occlulive methods (duct tape]
s-mt u.,. Thenlpia

Topical imiquimod
Bleomycin (inlrlllllliollll)*
Hypenensitivity Aglllls Dilitrochlorobenzene (DNCB) lmmu111 Response Modilin 5% imiquimod cream
Cornnon
Cornnon, planlll' Genital All Cornnon Cornnon, planlll' Flat Resistant Cornnon, planlll'
1binl U1111 Tbagpi CLRUage
Cautery
SLQerY Law Oral cnn.tidina (particularly chidran]
Topical Topical tretinoin (flat warts] Localized heat lllenpy lnlnllalional bleomycin (plllnlllr werts]
Mitcell1111111111 No treatment Salicylic acid 40% minimum Tnllinoin (topical)* Cimetidile (oral)* Duct tape occlusiorv'callous scrapinQI'parilg
'Awid in pragnuq
65-911'!1. resolve spontaneously over years Ovarthe counlar (DTC), use with occulsion Irritation Best in children C811tharidin + podophyllin + salicylic acid
.....
',.-----------------, '
Trallllllllnt far Anopaital W.rts
Fim 11111 thllfapies

lmiquimod 5% cra11111 PodophyDotoxin (solution, cream, or gel) PodophyDin rasin
Yeast Infections
CANDIDIASIS
Cryolharapy
Second IIIII tlllrapill Trichloroacetic acid Topica15-ftuo1111ncil
Eltctrodnsication Surgical excision (with cold steal or scissors]
Candida! Paronychia
painful red swellings of periungual skin management: topical agents not as effective; oral antifungals recommended macerated/eroded erythematous patches that may be covered with papules and pustules, located in intertriginous areas often under breast, groin, or interdigitally peripheral "satellite pustules predisposing factors: obesity, diabetes, systemic antibiotics, immunosuppression, malignancy starts as non-infectious maceration from heat, moisture and friction management: keep area dry, miconazole, ketoconazole/clotrimazole cream bid until rash clears
PITYRIASIS (TINEA) VERSICOLOUR
Candida! Intertrigo
chronic asymptomatic superficial fungal infection with brown/white scaling macules affected skin darker than surrounding skin in winter, lighter in summer (does not tan) sites: upper trunk most common
Pathophysiology
microbe produces carboxylic acid --+ inflammatory reaction inhibiting melanin synthesis yielding variable pigmentation affinity fur sebaceous glands; require fatty acids to survive
Etiology Pityrosporum ovale (Malassezia furfur)
also associated with folliculitis and seborrheic dermatitis predisposing factors: summer, tropical climates, Cushing's syndrome, prolonged corticosteroid use
Investigations
microscopic examination KOH prep of scales for hyphae and spores
Management
scrub off scales with soap and water selenium sulfide body lotion ketoconazole cream or PO daily for 10 days if more extensive
.....
''
Oral Tl!binllfina (LimisiP'] is not ellective because nis nat secnrted by sebaceous glands.
D32 Denoatology
Infections
Toronto Notes 2011
Sexually Transmitted Infections

SYPHILIS
Clinical Presentation characterized initially by a painless ulcer (chancre) following inoculation, systemic infection with secondary and tertiary stages Etiology
Treponema pallidum
transmitted sexually, congenitally, or rarely by transfusion
,,
Tabla 22. Stages of Syphilis

Primary Syplilis Clinical Presantmion Silgle red, indurated, painless chnre, that develops into painless ulcer with raised border and scanty serous exudate Chancre at site of ilocullllion after 3 weeks of D:ubation and h1111ls in 4-6 weeks; chancre may also develop on lips or anus Regional non-tender lymphadenopathy appears < 1 week after onset of chancre DDx: chancroid (painful), HSV (multiple lesions) Secondary Syphilis
Nllural Hiltory of Untrlllted Syphilil Inoculation Primary syphilis (1 B-90 daftsr infaction) Sacondll'( syphilis (simultanaous to primary syphilis or up to 6 mo after healing of primiiY lesion) Latent syphilis Tartillry syphilis [2-20 y)
Tartilry Syphilis
....
Lmnt Syphllil The period between healing of clinical lesions and appearance of 111111 miiiiDutions. 711'11. of untnsllllld patienb; will remain in this stage fur the mt of thair livaa and 11n1 immuna to new primary infection.
Presents 2-6 months after primary Extremely rare infection (patient may not recall 31 years attar secondary Main skin lesion: 'Gumma'- a of primary chancre) Associated with generalized granulomatous non-tender lymphadenopathy, splenomegaly, nodule headache, chils, fever, arlhralgias, myalgies, malaise, phatophobill Lesions heal in 1-S weeks and may recur for 1 year 3 types of lesions: 1. Macul85 and papul85: flat top, sceling, nan-pruritic, sharply defined, circular/annular rash (DDx: pityriasis rosea, tinea corporis, drug eruptions, lichen planus) 2. Condyloma lata: moist papules around genitaV peria1111l region 3. Mucous patches: macerated patches mainly found in oral mucosa
lnvatigations
CANNOT be based on dinical VORL positive presentation alone FTA-ABS +ve; -w after 1 year VORL negative- rapeat weekly following appennce of chancre for 1month Darklield +ve in all secondary Auorescent treponanal antibody-syphilis (FTA-ABSI test has jJ8ilter and may detect disease earlier in course Darklield examination spirochete in chancre fluid or lymph node aspirate Panicilin G, 2.4 million unils IM, single dose
As in prinary syphilis, WRL can be falsely negative
Mlnlg-11:
As far primary syphilis
Traalment: panicillin G, 2.4 million units IM weekly
GONOCOCCEMIA Clinical Presentation disseminated gonococcal infection hemorrhagic, tender, pustules on a purpuric/petechial background sites: distal aspects of extremities associated with fever, arthritis, urethritis, proctitis, pharyngitis and tenosynovitis neonatal conjunctivitis if infected via birth canal Etiology
Neisseria gonorrheae
Management notify Public Health authorities screen for other sexually transmitted infections (STis) cefu:ime 400 mg PO (drug of choice) or ceftria.xone 125 mg 1M
Toronto Notes 2011
Pre-Malignant Skin Conditioll8/Malignant Skin Thmours
Dermatology D33
Pre-Malignant Skin Conditions

actinic keratosis: 1-10% become squamous cell carcinoma (SCC) dysplastic nevi: risk of malignant melanoma (see Table 5}
Leukoplakia
Clinical Presentation a morphologic term describing homogenous or speckled white plaques with sharply demarcated borders sites: oropharynx, most often floor of the mouth, soft palate, and ventraUlateral surfaces ofthe tongue Pathophysiology precancerous or premalignant condition oral form is strongly associated with tobacco use and alcohol consumption Epidemiology 1-5% prevalence in adult population after 30 years of age; peak at age 50 M>F, fair-skinned most common oral mucosal premalignant lesion Differential Diagnosis lichen planus, oral hairy leukoplakia Investigations biopsy is mandatory because it is premalignant Management low risk sites on buccaUlabial mucosal or hard palate: eliminate carcinogenic habits, follow-up moderate/dysplastic lesions: excision, cryotherapy
Malignant Skin Tumours

Basal Cell Carcinoma (BCC)
--------------------------......
Subtypes noduloulcerative (typical} skin-coloured papule/nodule with rolled, translucent ("pearly"} telangiectatic border and depressed/eroded/ulcerated centre pigmented variant flecks of pigment in translucent lesion with surface telangiectasia may mimic malignant melanoma superficial variant flat, tan to red-brown plaque, often with scaly, pearly border and fine telangiectasia at margin sclerosing variant flesh/yellowish-coloured, shiny papule/plaque with indistinct borders Pathophysiology malignant proliferation ofbasal cells ofthe epidermis low grade cutaneous malignancy, locally aggressive (primarily tangential growth}, rarely metastatic usually due to UVB light, therefore >80% on face may also be caused by scar formation, radiation, trauma, arsenic exposure, or genetic predisposition (Gorlin syndrome) Epidemiology most common malignancy in humans 75% of all malignant skin tumours >40 years, increased prevalence in the elderly M>F, skin phototypes I and II, chronic cumulative sun exposure Differential Diagnosis benign: sebaceous hyperplasia, intradermal melanocytic nevus, dermatofibroma malignant: nodular malignant melanoma, sec
,...-----------------, ,
Wol'll-ql of Non11111lanoma Skin Cancer (NMSCI
HistDry: duration, growth rata, family/ personal hx of skin cancer, prior thanpy to the particular lesion.
Phyaiclll: location, &izu, whsther circumscriled, tethering to deep structures, full skiliXIIIIl, lymph node
axam
if shallow lesion do shave biop&y; othurwi&e punch biop&y.
.....
,.. ,
Margi Smallar liana: alectrodesicclllion and curatblge with 2-3 mm margin of normal skin. DHp mtiltratin IHiana: surgical excision with 3-5 mm margins beyond visible and palpable tumour border; may require skin graft or flap.
D34 Denoatology
Malignant Skin Tumours/Malignant Skin Tumours
Toronto Notes 2011
Management imiquimod 5% cream (Aldara) or cryotherapy is indicated for superficial BCCs on the trunk shave excision +electrodesiccation and curettage for all other types ofBCCs microscopically controlled, minimally invasive, stepwise exicison (Mohs surgery) or radiotherapy for lesions on the face or in areas that are difficult to reconstruct life-long follow-up 95% cure rate if lesion <2 em in diameter
Cutaneous T-Cell Lymphoma

Clinical Presentation Mycosis fungoides (limited superficial type) characterized by: erythematous patches/plaques/nodules/tumours, which may be pruritic and poikilodermic (atrophy, telagiectasia, hyperpigmentation) common sites include: trunk, buttocks, proximal limbs mildly symptomatic. usually excellent prognosis for early disease Sezary syndrome (widespread systemic type) rare variant characterized by: universal erythroderma ("redman syndromeD), lymphadenopathy, WBC >20 x 109/L with Sezarycells associated with intense pruritus, alopecia, palmoplantar hyperkeratosis, and systemic symptoms (fatigue, fever) often fatal Pathophysiology clonal proliferation of skin-homing CD4 T cells Epidemiology >50 years old, M:F 2:1 Differential Diagnosis tinea corporis, nummular dermatitis, psoriasis, discoid lupus erythematosus, Bowen's disease Investigations skin biopsy (histology, "lymphocyte antigen cella markers, TcR gene arrangement) blood smear looking for Sezarycells or flow cytometry(e.g. CD4:CD8 >10 is Sezary) imaging (for systemic involvement) Management Mycosis fungoides treatment is dependent on stage of disease topical steroids and/or PUVA, narrow band (311-313 mm), UVB (NBUVB) Sezary syndrome oral retinoids and interferon extra-corporeal photophoresis may need radiotherapy for total skin electron beam radiation may maintain on UV therapy
Malignant Melanoma (MM)
-----------------------------------------
Clinical Presentation malignant characteristics of a mole: see mnemonic "ABCDED sites: skin, mucous membranes, eyes, CNS
D-1his PaMnt h1011a Mu.. ur
Mal111011111?
.lAMA 1998; 279!91: 696-701
ABCDE c:hac:lclilt
Asymmlltry
Border {irragularl
Diameter (increasing or >6 mml Enlargement, elevation, evolution Sensitivity 92% (CI 82-96%1 Specificity 100% [CI 54-1 OO'lf.l
Colour !Vllriudl
Subtypes of Malignant Melanoma lentigo mallgoa malignant melanoma in situ (normal and malignant melanocytes confined to the epidermis) 2-6 em, tan/brown/black uniformly flat macule or patch with irregular borders lesion grows radially and produces complex colours sites: face, sun exposed areas 1/3 evolve into lentigo maligna melanoma lentigo maligoa melanoma ( 15% of all melanomas) malignant melanocytes invading into the dermis associated with pre-existing solar lentigo, not pre-existing nevi flat, brown, stain-like, gradually enlarging with loss of skin surface markings with time, colour changes from uniform brown to dark brown with black and blue found on all skin surfaces, especially those often exposed to sun
Toronto Notes 2011
Malignant Skin Tumours
Dermatology D35
superficial spreading melanoma (60-70% of all melanomas) atypical melanocytes initially spread laterally in epidermis then invade the dermis irregular, indurated, enlarging plaques with red/white/blue discolouration, focal papules or nodules ulcerate and bleed with growth nodular melanoma (30% of all melanomas) atypical melanocytes that initially grow vertically with little lateral spread uniformly ulcerated, blue-black, and sharply delineated plaque or nodule rapidly fatal acrolentiginous melanoma (5% of all melanomas) ill-defined dark brown, blue-black macule palmar, plantar, subungual skin melanomas on mucous membranes have poor prognosis Pathophysiology malignant neoplasm of pigment forming cells (melanocytes and nevus cells) Epidemiology incidence 1:100 risk factors: numerous moles, fair skin, red hair, positive personal/family history, large congenital nevi, familial dysplastic nevus syndrome most common sites: back (males), calves (females) worse prognosis if: male, on scalp, hands, feet. late lesion, no pre-existing nevus present Differential Diagnosis benign: nevi, solar lentigo, seborrheic keratosis malignant: pigmented BCC Management excisional biopsy preferable, otherwise incisional biopsy remove full depth of dermis and extend beyond edges oflesion only after histologic diagnosis beware oflesions that regress - tumour is usually deeper than anticipated lymph node dissection shows survival advantage if nodes uninvolved chemotherapy (cis-platinum, BCG), high dose interferon for stage II (regional) and stage III (distant) disease radiotherapy may be used as adjunctive treatment
Table 23. American Joint Committee on Cancer Staging System Based on Breslow's Thickness of Invasion
T1 <1.0mm T2. 1.01-2.0 mm T3 2.01-4.0 mm T4 >4.0mm Stage I T1a- T2a Stage II T2b -T4b Stage Ill any nodes Stage IV any melll 5-year survival 911% 5-year survival 711% 5-year survival 45% 5-year survival 1ll%
11:1
Risk Factors fer Mellnom no SPF in SIN Sun exposure Pigment hits {blue eyes, fllir/red hl.ir, pale complaxion) Fraclding Skin reaction to sunligtrt {increuad incidence of sunburn) lmm111osuppressive states {e.g. renal 1nnsplantation) Nevi (dysplastic nevi; increased number of benign malanocytic nevi)
... , ,
Node Dissllction lor LlsioM > 10 mm Assess sentinel nodes If macroscopically or microscopically positive, a lymph node dissection should be prefonned prior to wide excision of 111e primarv melanoma to ensure accurate lymphatic mapping.
.-----------------,
a = no ulceration; b = ulceration
Squamous Cell Carcinoma (SCC)
----------------------
Clinical Presentation indurated erythematous nodule/plaque with surface scale/crust. and eventual ulceration more rapid enlargement than BCC sites: face, ears, scalp, forearms, dorsum of hands Pathophysiology malignant neoplasm ofkeratinocytes (primarily vertical growth) predisposing factors include: UV radiation, PUVA, ionizing radiation therapy/exposure, chemical carcinogens (such as arsenic, tar and nitrogen mustards), HPV 16, 18, immunosuppression Epidemiology second most common type primarily on sun-exposed skin in the elderly, M>F, skin phototypes I and II, chronic sun exposure in organ transplant recipients sec is most common cutaneous malignancy, with increased mortality Differential Diagnosis benign: nummular eczema. psoriasis, irritated seborrheic keratosis malignant: keratoacanthoma, Bowen's disease, BCC
D36 Denoatology
Malignant Skin 1\unours/Alopecla (Hair Lou)
Toronto Notes 2011
Management surgical excision with primary closure, skin flaps or grafting lifelong follow-up (more aggressive treatment than Bee) Prognosis good prognostic factors: immediate treatment, negative margins, and small size of lesion sees that arise from actinic keratosis metastasize less frequently (-1 %) than other sees (e.g. arising de novo in old burns) (2-S% of cases) overall control is 7S% over 5 years, 5-10% metastasize
BOWEN'S DISEASE (SQUAMOUS CELL CARCINOMA IN SITU)
Clinical Presentation erythematous plaque with a sharply demarcated red and scaly border often 1-3 em in diameter and found on the skin and mucous membranes evolves to sec in 10-20% of cutaneous lesions and >20% of mucosal lesions Management same as for Bee biopsy required for diagnosis topicalS-tluorouracil (Efu.dex) or imiquimod (Aldara) used if extensive and as a tool to identify margins of poorly defined tumours shave excision with electrodesiccation and curettage
Alopecia (Hair Loss)

Hair Growth
It'
lllirl.nl TOP HAT Telogen ElflwiLm, tilea capitis Out of Fe,ln Physical"com-row" bnliding Hormonal- hypothyroidism, androgenic Autoimmune- Slf, Tmcins- huvy mltll1, anticoeguillnts, chemothanpy, V"lt A, SSRI1
hair grows in a cyclic pattern that is defined in 3 stages 1. growth stage = anagen phase
2. resting stage = telogen phase 3. degenerative stage = catagen phase total duration of the growth stage reflects the type and location of hair: eyebrow, eyelash, and axillary hairs have a short growth stage in relation to the resting stage growth of the hair follicles is also based on the hormonal response to testosterone and dihydrotestosterone (DIIT): this response is genetically controlled
Non-Scarring (Non-Cicatricial) Alopecia

PHYSIOLOGICAL
Clinical Presentation male-pattern alopecia (androgenic alopecia) fronto-temporal areas progressing to vertex, entire scalp may be bald Pathophysiology action of testosterone on hair follicles Epidemiology early 20's-30's (female androgenic alopecia is diffuse and occurs in 40's and SO's) Management minoxidil (Rogame) lotion to reduce rate ofloss/partial restoration spironolactone in women (anti-androgenic effects), cyproterone acetate (Diane-3s) finasteride (Propecta) (S-a-reductase inhibitor) 1 mgld in men hair transplant
PHYSICAL
trichotillomania: impulse-control disorder characterized by compulsive hair pulling with irregular patches of hair loss, and with remaining hairs broken at varying lengths traumatic (e.g. tight "com-row" braiding of hair)
Toronto Notes 2011
Alopecia (Hair Loss)
Dermatology D37
TELOGEN EFFLUVIUM
uniform decrease in hair density secondary to an increased number of hairs in resting stage (telogen stage)
......
'
follicl1111 on IIXIIm -+ biopsy not requillld. Scring lllupecill: llbsent hair follicles on IIXIIm -+ biopsy raquinld.
Non--rma ICIIIICia: intact hair
Pathophysiology precipitated by: malnutrition, Fe deficiency, thyroid dysfunction, post-partum/miscarriage,

scalp diseases (seborrheic dermatitis, allergic contact dermatitis), medications (e.g. OCP), physical!mental stress, Fe deficiency hair loss typically occurs 2-4 month after exposure to precipitant regrowth occurs within a few months but may not be complete
......
DDx of No1HC8rring Alopeci
Aulnimmune Alopacill arealll Endocrine
ANAGEN EFFLUVIUM
hair loss due to insult to hair follicle impairing its mitotic activity (growth stage)
Hypotllynoidism
Androgens Micronutrient deficienci1111
Iron
Zinc Toxins Heavy rnebU Anticoagullllll Chemo1herapy VrtaminA
Pathophysiology precipated by chemotherapeutic agents (most common}, other meds (bismuth.levodopa,

colchicine, cyclosporine}, exposure to chemicals (thallium, boron, arsenic) dose-dependent effect hair loss 7-14 days after single pulse of chemotherapy; most clinically apparent after 1-2 months reversible effect; follicles resume normal mitotic activity few weeks after agent stopped
Trauma to 1he hair follicle

Trichotllomanill 'Com-row' bniding Other Severe illn8SS
Childbirth
ALOPECIA AREATA
autoimmune disorder characterized by patches of complete hair loss localized to scalp, eyebrows, beard, eyelashes alopecia totalis -loss of all scalp hair and eyebrows alopecia universalis -loss of all body hair associated with dystrophic nail changes - fine stippling "exclamation mark" pattern (hairs fractured and have tapered shafts, i.e. looks like "!") may be associated with pernicious anemia, vitiligo, thyroid disease, Addison's disease spontaneous regrowth may occur within months of first attack (worse prognosis if young at age of onset and extensive loss) frequent recurrence often precipitated by emotional distress
Management
generally unsatisfactory intralesional triamcinolone acetonide (corticosteroids) can be used for isolated patches UV or PUVA therapy imm.unomodulatory (diphencyprone)
......_._______________ '
DDx of Sallmlg (aianlcill Alopellill
Scarring (Cicatricial) Alopecia

irreversible loss ofhair follicles with fibrosis
Developmenmi/Heredilary Disorders
Aplasia cutis conganila Epidennal nevi Romberg's ryndr011111 Genlnllized follicLJar hamartoma Primary caus1111
Etiology
physical: radiation, bums infections: fungal, bacterial, TB, leprosy; viral (herpes zoster) inflammatory lichen planus (lichen planopilaris} discoid lupus erythematosus (DLE} (note that SLE can cause an alopecia unrelated to discoid lupus lesions which are non-scarring) morphea: "coup de sabre" with involvement of centre of scalp
Group 1: Lymphocytic
Lupus urythematosus Lict.n plllnopillris
Clllnic Pseudopalllde Group 2: Neutrophilic

FoUiculitis declllvans
Group 3: Mixlld
Acne k!loidalis nuchae Secondary C8USIIS Infectious agents Bacturial (i.e. post-callulitis) Fungal (i.e. tinea capitis) Neopla&ma (i.e. BCC, SCC, Lymphomas, and metastatic Physiallagants Mechanical tnuma Bums
Investigations
biopsy from active border
Management
infections: treat underlying infection inflammatory: DLE treated topical/intralesional steroid or antimalarial
Radiotherapy C-uatic chemicals
D38 Denoatology
Nails and Disorders of the Nail Apparatus
Toronto Notes 2011
Nails and Disorders of the Nail Apparatus

Table 24. Nail Changes in Systemic and Dennatological Conditions
Nil Abna11111lity
Dafinition/EtioiiJIW
Associltld DiISI
Cyanotic heart disease. bacterial endocarditis. pulmonll'( disorders, Gl disorders, etc.
NAIL PLATE CHANGES

Clubbing Kaiiiiii'{Chia Onycholysis Onychogryphosis Onychohemia Onychomycosis Onychocryptosis (III!J1IWII toenail Proximal nail plate has greal!!r 1han 180 degree to nail fold, watch"{llass nails, bLJbous digils Spoon shaped nails Sepanrtion of nail plate from nail bed Hypertrophy of 1he nail plate and subungal hypertenrtosis SubuiiiJIIII hematoma Fungal iriaction of nail (e.g. dermatophyte, yeast. mould) Often hallux with congenital malalignment. painfij inflammation. granulation tissue Distal margn has v-shaped indentation Distal nail plate does not sapanrte from nai bed Punctate depressions 1hat migrate distally with growth
11111 deficiency, malnutrition, dillbsllls

Psoriasis, dermatophytes, thyroid disease Poor circLJation, chronic irlllmnation, tinea Trauma to nail bed HIV, diabetes, piii1Jheral arterial disease light fittilll shoes, excessive nail clipping
SURFACE CHANGES
Wedge shaped Darier's disease (follicular dyskeratosis) Scleroderma Psoriasis, alopecia areata. eczema
Pterygium inversus unguium

l'itlilg
Transverse ridging Transvene white lines
of nail plate
COLOUR CHANGES
Yellow Green Black Brown Splirter hemorrhages
Transverse depressions often more in central portion Serious acute illness slows nail growth (Beau's Iiles), eczuma, chronic paronychia. trauma Poisons, hypoelbuminemia (Muhetb's lines) linea, jaundice, telracycline, pityriasis rubra pilaris, yellow nail synome
Bands of white discalouration
Pseudomonas
Melanoma, hematoma Nicotine use, psoriasis, poisons Extravasetion of blood from longitudinal vessels of nai bed Blood attaches to nail plate and moves distally as it grows Brown-yellow discolouralian HSV infection of dstal phalanx Local inflammation of 1he nail fold around the nail bed Cuticular hemorrhages, roughness, capillary chang as Trauma, bacterial endocarditis, blood dyscrasias, psoriasis
Oil spots
Psoriasis Gerital herpes infection
NAIL FOLD CHANGES

Herpetic whitlow Paronychia
Acute: painful infection

Chronic: constant wetting {e.g. dishwashing, thumbsuckilll) Scleroderma, SLE
Nail fold telangiectasias
Toronto Notes 2011
Skin Manifestations of Systemic Disease
Dermatology D39
Skin Manifestations of Systemic Disease

Tabla 25. Skin Manifllltationa of Internal Conditions
Dilell8
Rallllld D1111111Du1
Painful apthous ulcers in oral cavity genital mucous membrales, erythema nodosum Superficial migratory thnontophlebitis. cyanosis, gqrene, ulcerations
It'
AUTOIMMUNE DISORDERS
Behs disease Buerger's disease Dermatomyositis
Periorbital and perioral violaceous erythema, heliotrope with edema. Gottron's papules (violaceous ftat-topped papules with atrophy), periungual erythema, telangiectasia, calcinosis cutis Polyarbritic noll.IIB5, &t&llirte purpura, urytherna, gangrena, 5plirt11r hamanhages, liwdo raticula'is Petechiae, urticaria, erythema nodosum, rheumatic noWies Raynaud's, nonpitting edema, waxy/shiny/tense atrophic skin (morphea), ulcers, cutaneous calcification. periungual telangiectasia, acrosclerosis Malar erythema, discoid rash (erythematous papules or plaques with keratotic scale, follicular plugging, atrophic scarrilg on face, hillds, and anns), hemonhagic bulae, palpable purpura, urticarial purpura, patchy/diffuse alopecia, mucosal ulcers, photosensitivity Pyudlll'rll8 gangrano&UIIl, erythBillB nodosum Genaralized hyperpigmentation or limitad to skin folds, buccal mucosa and scars Moon facies, purple sbiae, acne, hyperpigmentation, hirsutism, atrophic skin with telangiectasia Infections (boils, carbuncles. Cllldidiasis, S. aureus, dermatophytoses. tilea pedis 111d cruris, ilfectious eczematoid dermatitis), pruritus. eruptive xanthomas, necrobiosis lipoidica diabaticorum, granuloma annulare, diabatic foot. diabBtic bulaa, acanthosis nigricans, calciphylaxis Moist warm skin, seborrhea, acne, nail atrophy, hyperpigmentation, toxic alopecia, pretibial myxedema, acropachy, onycholysis Cool, dry, scaly, thiclrBned, hyplll'pigmented skin; toxic alopecia with dry, coarse hair, brittle nails, myxedema, loss of lateral1/3 eyebrows
Rayu.ud's Phllno11111nan DDx

COlD HAND Cryoglobulini;/Cryofibrinogans ObstructioWOccupationll Lupus arythamatasus, other connective tiuue disease Diabstes mallitulllllrugs Hematologic problams (polycythamia, leukemia, ell:) Arterial problems (alherosclerosis) Neurologic problems (vascular tone) DiseiUIII of unknown origin !idiopathic)
Polyarteriti& nodO&a
Rheumatic fever Scleroderma Systemic lupus etylhematosus
Ulclllllliw colitis (UC)
ENDOCRINE DISORDERS
Addison's disease Cushing's syndrome Diabetes mellitus
...._' I
9,.-----------------,
Acantholis Nigrit:An asymptamatic dar1t thickened velvety hyparpigmantation of fiBXIIral skin most commonly around the neck. Associated
Hyperthyroidism Hypothyroidism HIV-RELA'IED Infections
with diabstes, obesity and other
endocrine disorders and malignancy. It is a cutanaous marbr of tissue insulin resismnce.
Viral (HSV. HZV, HPY. cytomegalovirus, molluscum contagiosum, oral hairy leukoplakia), bacterial (impetigo, acneiform folliculitis. denllll caries, cellulitis, bacillary epithelioid angiomatosis, syphilis), ather (candidiasis)
Seboi'Thea, psoriasis. pityriasis rosea, vasculitis
lnftammatory dermatoses Malignancies
Kaposi's sarcoma, i'r'n1Jhoma, BCC, SCC, malignant melanoma
MAUGNANCY
Adenocarcinoma Gastrointestinal (Gil Cervix/anus/rectum Cancinoma Breast Gl Thyroid BrearVGU/IunQ/DVllry Peutz-Jeghars: pigrnanted maculas on lipli/oral mucosa Paget's Disease: eroding scaling pla!Jies of perineum Paget's Disease: eczematous and crusting lesions of breast Palmoplantar keratoderma: thickened ski1 of palmli/soles Sipple's SyncRma: multiple mucosal neuromas Dlll'llllltomytJ8itis: heliatropa of ayalids and purplish plaquas DVllr knucldas Ataxia Telangiectesia: telangiectasia on pinna, bulbar conjunctiva Ichthyosis: generalized scaling especially on extremities Bloom's syndrome: butterfly etylhema on face, associated with short stature Amyloidosis: la11Je, smoath tongue with waxy papules on syelids, nasolabii111olds illd lips, as well as facial petechiae
Acute Leukemia
Multiple Myaloma
DTIIERS
Liver disease
Pruritus, hyperpigmentation. spider lle'Ji, palmar erythema, while nails (Terry's nails), porphyria cutanea tarda, xanthomas, hair loss Pruritus, pigmentation, half and half nails
Erythematous papules or urticarial plaques in distribution of striae distensae: buttocks, thighs, upper inner arms and lower backs Palpable purpura in cold-exposed areas. Reynaud's, cold urticaria, acral hemorrhagic necrosis, bleeding disordars, associated with hepatitis Cinfection
Renal disease
Pruritic urticaria papules and of pregnancy Cryoglobulinemia
D40 Denoatology
Pecliatrlc: E:unthems
Toronto Notes 2011
Pediatric Exanthems
It'
Itchy Eruptione il Childhood
Definitions exanthem: an eruption on the skin occuring as a symptom of a systemic disease typically with a fever enanthem: an eruption on a mucous membrane occuring in the context of an exanthem Table 26. Common Pediatric Exanthem
Eunthem Etiology
Human herpes virus (HIN)3 Incubation 10-2.1d, Communicable 1-Zd Pre-rash to Sd post-rash Clilicalllelcription Diffuse vesicular pustular beginning on thorax spreading to lmpoltant Co11plication Necrotizing fasciitis, er.:ephalitis, cerebellar ataxia, disseminated intravascular coagulation (DIC), hepatitis Supportive therapy, Acyclovir severe, Varicella Zoster immunoglobulin (within 96 hrs Dl contact), Varicela vaccine Supportive care mr majority Serious cases (irrmunosuppriiBSed) can be 1ntated pleconaril No 1reatnur1t: clildren oftan feel wall NSAIDs mr symptomatic arthropathy
UC-SCAB
Urticaria Canlllct dermatitis
Scabies Chicksn pox Atopic dennatitis

Bitn
New lesions wery Enanthems
Entarovhl
EnllrDviruses Polymorphous rash None Most conmon exanthem (macules, papules, vesicles, in summer and fall pBIBchiae, urticaria) Plrvavirus 819 Slapped cheeks (rad, Incubation 4-14d flushed cheaks)then Paaks in winter and sprilg 1-4 days IIIIer lacy/raticular maculo-papular rash Dl trunlr/axtremities STAR complex (Sore Tlroat, Artllilis, Rash) Fetal infection (anemia. fatal hydrops or death) Aplastic crisis in siclde cell patients None
Erythema
lnfectiolum
Gilnafti.Cnllti Epstein-Bill virus most Symmetric papular Synd111111 conmon, hepatitis B, of face, buttocks, cDXSaCkie, parvovirus and extremities Spring and early summer
Hand, Foot
Supportive treatment
and Malllll Disalltl

Kawasaki
Coxsackie A and Bviruses Vesicular eruption Dl Hijiy contagious virus palms and soles with an erosive stomatitis No proven viral etiology, but infllctious etiology suggested Superantigen toxin mediated bacterial process proposed Late wilter to spring l'lnnyxovirus Incubation 10-1 4d Communicable 4d before and after rash
Pulmomry, neurological death
Supportive treatment
Disa11t1
,.....
Fever> 5 days and 4/5: Most common cause of Aspirin, intravenous unilateral lymphadenopathy; vasculitis and acquired immunoglobulin, baseline pufty/red palms and soles; heart disease in clildren echo and repeat in 6 weaks red, cniCked lipt/strawberT'f CNS, Gllnlct, kidney, eyes tongue; skin rash; non purulent bilateral conjunctivitis Erythematous macular beginning on head and spreading downwards, deslJlllmeteS. no palm or sole involvement Enanthem: Koplik spots (grey/white papules on buccalll'lJcosa) Pink maculss and papulas on trur*. neck. pnlXimal extremities, and occasionally face Eruption aftEr high fever ends 1-5 daysmllowing mild prodrome /lever, headache, respiratory symptoms), a pink maculo-papular rash erupts on face Slfl!llding in a caphalocaudal direction Occipital and nrtroauricular nodas Otitis media. pnewnonia, er.:ephalitis, SJS, glomerular nephritis, Vitamin A. irrmunoglobulin, measles/ITIJII1ps/rubella (MMR) vaccine
RaiiiCIII
HHV6,HHV7 Incubation 9-1 Od
Neurological involvement Viral reactivation in immunosuppressed patients STAR complex Congenital rubella (cataract, glaucoma. thrombocytopenia, hepatitis, deafness. congenital heart disease)
Supportive treatment Antipyretics during 1he febrile pariod
Rubella
RNA virus Dlthe Togaviridae famly Incubation 16-1 8d
Supportive treatment MMR vaccine Serologic testing in rubellaexposed pregnant women
Scarlet Fever Group A beta-hemolytic

streptococci toxin types A, B,and C Late fall, winter, and
Generalized rash, red Mastoiditis, otitis, sinusitis, 10-1 4 day course of papules, sand-paper" pneumonia, meningitis, penicillin myocarditis, arthritis, textura, dasquamation. hepatitis, rheumatic fever, flexural accentuation, enanthem {strawbeny and gomerulonephmis tongue. petechiae on palate) Pastia's Iiles -linear petechial streaks i'1 axillary, and antecubital ereas
Toronto Notes 2011
Dermatology D41
Miscellaneous Lesions
Angioedema and Urticaria
Angioedema
deeper swelling of the skin involving subcutaneous tissues; often involves the eyes, lips, and tongue may or may not accompany urticaria hereditary or acquired forms hereditary angioedema (does not occur with urticaria) onset in childhood; 80% have positive family history recurrent attacks; 25% die from laryngeal edema triggers: minor trauma, emotional upset, temperature changes treatment prophylaxis with danazol or stanozolol epinephrine pen to temporize until patient reaches hospital in acute attack
......
.. ,
Whaal Typically arythamalllus flat-lllppad, palpable lesions wrying in size circumscribed dermal edema lndividlllllesion lasts < 24 hrs Associated with mast cell release of histamile May be pruritic
Urticaria
also known as "Hives"; see Table 27 for classification transient, red, pruritic well-demarcated wheals each individual lesion lasts less than 24 hours second most common type of drug reaction results from release of histamine from mast cells in dermis can also result after physical contact with allergen
Tabla 27. Classification of Urticaria
Acute Urticaria >2/3 of cases Attacks last <6 weeks Individual lesions last <24 In
Drugs - especially aspirin. NSAIDs Foods - nuts, shellfish, eggs, fruit Idiopathic Infection
IE'
DDx fur UrtiCllria
Insect stings
Percutanous absorption - cosmetics, wart exposures
Stress
Systemic disiiiiSes - systemic lupus erythBilllltosis {SL.E], endocrinapathy, neoplasm
Ch11111ic Ullicaril
<1/3 of cases
Attacks last >6 weeks Individual lesion lasts <24 In
lgE-dBP&ndent: trigger associated Idiopathic {90% of chronic urticeria patients! Aeroallergens Drugs {antibiotics, honnones,locellllestheticsl Foods and additives Insect stings (bees, wasps, homstsl Parasitic infections Physical contact (animal saliva, plant resins, latex, metals, lotions, soap) Direct mast cell release Opiates, muscle reiiiXllnts, radilt-contrast agents Corl1Jiement-mediated Senun sickness, transfusion reactions Infections. vira[lbacterial ( >110% of urticaria in pediatric patientsI Urticarial vasculitis Arachidonic acid metabolism ASA,NSAIDs Physical Dennatographism (friction, rubbilg skinl, cold (ice cube, cold waterl. cholilergic (hat shower, exerciseI. solar, pressure (shoulder strap, buttocks!. aquagenic (exposure to water), adrenergic (stress!, heat
DAM HIVES Drugs and loads Allergic Malignancy Hereditary Infection Vasculitis Emotions Stings
......
Approach to Urticaria 1. Thorough Hx and P,ll: 2. Acute: if individual lesions last < 24 hours, but IIIW:ks last <6 weeks; no immediate investigllions needed; consider for allegy te5ting 3. Chronic: if individual lesions last < 24 hours but attacks lui > 6 weeks; further invastigations roquirad: CBC+diff, urinaiY$il. ESR, LFTslll help identify underlying causa 4. Vuculitic: if individual lesions last > 24 hours; biopsy of lesion and dennatology
Other Mastocytosis, Llticllia pigmentosa

lndividuallesioll51ast >24 In nan.puritic Requires biopsy
lluculilic Urtic:aria
Idiopathic Infections Hepatitis

Autoirrrnme diseases
..... ,
M..tacytoU. (Urticaria PigmentlllaJ Rare dilene due tc IIXCenive infilbation of the skin by mast calls. It manifests as many reddiah-brown ellllllllad plaques and maculas. Applying prassu111 tc a lesion produces a whell surrounded by intansa erythema (Dariar's sign), due tc mast cell degranulation. This occtn within minute..
SLE Drug hypersensitivity cimetidine and
D42 Denoatology
Miscellaneous Lesions
Toronto Notes 2011
Erythema Nodosum

----------------------------------------
acute or chronic inflammation of subcutaneous fat (panniculitis) round, red, tender, poorly demarcated nodules sites: asymmetrically arranged on lower legs, knees, arms associated with arthralgia, fever, malaise
Etiology
DDx of Erythema Nodoe1m
NDDDSUM No cause [idiopmhic) in 40% Drugs [sutfonamidas, OCP, ate.) Other inflctions [GAS+) Sarcoidosis Ulcerative colitis and Crolvl's Malignancy [leukemia, Hodgkin's lymphoma)
40% are idiopathic drugs: sulfonamides, oral contraceptives (also pregnancy), analgesics, trans retinoic acid infections: GAS, primary tuberculosis (TB), histoplasmosis, Yersinia inflammation: sarcoidosis, Crohn's > ulcerative colitis malignancy: acute leukemia, Hodgkin's lymphoma
Epidemiology 15-30 years old, F:M = 3:1

lesions last for days and spontaneously resolve in 6 weeks
Investigations
chest x-ray (to rule out chest infection and sarcoidosis) throat culture, antistreptolysin (ASO) titre, purified protein derivative (PPD) skin test
Management
symptomatic: bed rest, compressive bandages, wet dressings NSAIDs treat underlying cause
Pruritus
a sensation provoking a desire to scratch pruritis can present with or without skin lesions lesions may arise from the underlying disease, or from excoriation causing crusts, lichenified plaques, or wheals
It'
Etiology
dermatologic - generalized asteatotic dermatitis ("winter itch) pruritus of senescent skin (may not have dry skin, any time of year) infestations: scabies, lice drug eruptions: ASA, antidepressants, opiates psychogenic states dermatologic -local atopic and contact dermatitis, lichen planus, urticaria, insect bites, dermatitis herpetiformis infection: varicella, candidiasis lichen simplex chronicus prurigo nodularis systemic disease - usually generalized hepatic: obstructive biliary disease, cholestatic liver disease of pregnancy renal: chronic renal failure, uremia secondary to hemodialysis hematologic: Hodgkin's lymphoma, multiple myeloma, leukemia, polycythemia vera, hemochromatosis, Fe deficiency anemia, cutaneous T-celllymphoma neoplastic: lung, breast, gastric (internal solid tumours) endocrine: carcinoid, DM, hypothyroid/thyrotoxicosis infectious: HIV, trichinosis, echinococcosis, hepatitis C psychiatric: depression, psychosis neurologic: post-herpetic neuralgia, multiple sclerosis
DDx of Pruritu
SCRATCHED ScabiN Cholestasis Banal Autoimmune Tumours Crazies (psychiatric) Hematclogy [polycythemia. lymphoma)
Endocrine (thyroid. parathyroid, ..V Fe) Drugs, dry skin
Investigations
detailed history complete physical, including rectal and pelvic examination bloodwork: CBC, ESR, Cr/BUN, LFT, TSH, fasting blood sugar, stool culture and serology for parasites
Toronto Notes 2011
Miscellaneoua Lesions/Common Medications
Dermatology D43
Management
treat underlying cause cool water compresses to relieve pruritus bath oil and emollient ointment (espedally if xerosis is present) topical corticosteroid and antipruritics (e.g. menthol, camphor, phenol, mirtazapine, capsaicin) systemic antihistamines: Hl blockers are most effective, most useful for urticaria phototherapy with UVB or PUVA
Wounds and Ulcers

Tabla 28. Diffarant Typas of Ulcars and Traatmant
Ulcer Type
Arterial
Cliniclll'nlsemtion
Wlund ill lip& uf toB5, cold feet with claudication, gangll!lle, distsl hypenmia, decreased pedal pulses Doppler &tudy If ankle:brachialmtio <0.4, cCIISider amputation If gangrenous, paint with betadine Otherwise, dressings to promote moist inlerllc1ive wound healing
Uncommon Cau- of Ulcers
CHIP IN Cancar, chrom0101118.1

Hemoglobinopathy
Inflammatory
Pyoderma gangrenosum Infections Necrobiosis lipoidica diabeticorum
Wlund at malleolus, stasis change, edema, Local wound dressing: moist iniBllctive healing previous venous i!lury Compression: preferably four layers After wound heals, suwort stockings for lit& Nratropic and Diabetic llllculitic Wlund ill prassura point or secondary to unknown trauma. common at base uf 1st metatarsal phalangeal (MTP) Livedo reticularis, petechiae, extreme tenderness, delayed healing
Prassura downloading by usilg proper sho8f/s8ills Promote moist irrteractiva wound healing Appropriate broad-spectrum arrtibio'lic cDVerage
Biopsy to determine Serum screening for vasculitis Treat vasculitis Local moist irteractive healing
.....
.. ,
antimicrobials
Key to I Wound tlllt doll Nat Hill ...
llelenllaA dabridemant of biofilm and

8iopay lll1'f wound without siiJIII of healing altar 3 months to rule out
CIIICerl
Common Medications
Sunscreens and Preventative Therapy
Sunburn erythema 2-6 hours post UV exposure often associated with edema, pain and blistering with
subsequent desquamation of the dermis, and hyperpigmentation chronic UVB exposure leads to photoaging, immunosuppression, photocardnogenesis prevention: avoid peak UVR (10 am to 4 pm), wear appropriate clothing, wide-brimmed hat, sunglasses, and broad-spectrum sunscreen clothing with UV protection expressed as UV protection factor (UPV) is analogous to SPF of sunscreen
.....
,
UVBorWC
uv Radlltian
UVA (3Z0-4011 nmJ: Aging Penetrates skin more effectively 1han
Sunscreens
sun protection factor (SPF): under ideal conditions an SPF of 10 means that a person who normally burns in 20 minutes will burn in 200 minutes following the application of the sunscreen topical chemical: absorbs UV light requires application at least 15-60 minutes prior to exposure, should be reapplied every 2 hours (more often if sweating, swimming) UVB absorbers: PABA, salicylates, cinnamates, benzylidene camphor derivatives UVA absorbers: benzophenones, anthranilates, dibenzoylmethanes, benzylidene camphor derivatives topical physical: reflects and scatters UV light titanium dioxide, zinc oxide, kaolin, talc, ferric chloride and melanin all are effective against the UVA and UVB spectrum less risk of sensitization than chemical sunscreens and waterproof, but may cause folliculitis or miliaria some sunscreen ingredients may cause contact or photocontact allergic reactions, but are uncommon
Responsible for tanning, burning, wrinkling and pl8mllluru skin aging Penetnrtes clouds. gl- and is ruftac:l&d off Wlltar, 1110w lllld carnant
UVB (ZIW20 nmJ: laming Ablorbed by 111e out&r dermis Is mainly responsible for burning and p18mlllu18 skin aging tor BCC, sec Dan not p811111nrte gl11111 and is substantially absorbed by ozone
UVC (ZO&-ZIU nml Is fillll'ld by olllllellyar
Management sunburn: if significant blistering present, consider treatment in hospital; otherwise, symptomatic
treatment (cool wet compresses, oral anti-inflammatory, topical corticosteroids) antioxidants, both oral and topical are being studied for their abilities to protect the skin; topical agents are limited by their ability to penetrate the skin
D44 Denoatology
Common Medications
Toronto Notes 2011
..... '
....mv. Percutann .._,lllitln
Fornnn 1.0 1.7
3.7 6.0
13.0 42.0 Body Site:
Topical Steroids
Tabla 29. Potency Ranking of Topical Steroids
Ralllin Patency
Welk
Rallllive Strtlngth
x1
x3
G..ric Nm
hydrocortisone 1% hydrocortisone 2% 17-valeme- o.Z'l. dasonide mDI1IBtllsone furorata bstamsthasona - 0.1% 11-valeme - 0.1% ncinonide betamethasone dipropionate - 0.05% fluocinonide - 0.05% clobetasol propionate (mo&t potentl betamethasone dipropionate ontment halobetasol propionate
Tl'llla Na11111
UMgl
ntertriginous !l'eiiS, clildren. face, thiukin Arm, leg, tJUnk
Plantar fuat Palm BliCk Scalp Forehllld Cheeks Scrolum
0.14 0.83
Modanrlll
Tridesilon Bacornat Batnoval88 Celestodenn -vat Diprosonellt Lidex, Topsyn ger' Lydannat Body
Patent
x6
Calculation of strangth of staroid compared 1D hydrocortisone on fo1'811111: relative strength of staroid x ralllliva
pwcutaneousllbsO!p!ion
Very Patent
Extr.nely Potllnt
x9
Palms 111d soles
....
''
Steroid acne
ROMCII
x12.
Dennovate8
Diprol-at
Palms 111d soles
Side Efflcts of Topical Sttroldl 1. Local: A1rophy Plrionll dl!llllllitis

Contact Tachyphylaxis {tolanncaf 2. Sysmmic: of HPA axis
Dermatologic Therapies
Tabla 30. Topical Therapies that are Important in Dematology D11111 Nama Dosing Schala lndicllliC.lcipotriol (Dovan..-1
0.005% cream, ointment. scalp Psoriasis
solution, apply BID For maintenance DD
Cammants
Burning, itching, skin irritation, worsening of psoriasis Avoid face, rrucous mentranes, eyes; wa&h hand& after Maximum weekly dosage of cream by
2.-5 years - 2.5 !Vwk 6-10yaars- 50 WWk 11-14 years- 7511fwk >14 years-100 glwk
lmiquimod (Aiduall] Genital warts 5% cream applied 3llfwk at bedtime, leave on Cutaneous warts 6-10 hours, 1han wash off with Actinic keratosis mild soap and water Max. ckuation 16 weeks Superficial basal call carcinoma Avoid naturaVartificial sun exposure Local skin and application site reactions
age:
Erythema,
edema,
sympllms Works best for warts on mucosal surfaces May induce inllammation and erosion
(Kwelllda41 P Lotion and Dennal C1111m)
Parmatl11i1
....
,...----------------. ,
greasy
5% cream, applied once Scabies (Kwellada-P Lotion, DVIII11ight to all skin areas torn NiJ:8 Dermal Cream) neclkdown Padiculosis (ICwallad&-P Cnina Nix Crime Rinse411 1.0% cream BID
Usa for as long a& lesions pa1$ist and die upon resolution of symptoms Atopic dennatilis (mild to moderate)
Do not use in children <2 vrs old Hypersensitivity to drug, or known sensitivity to chrysanthemums Local reactions only (resolve rapKJvl; including burning, pruritis Low toxicity, excellent results Consider 2nd application after 7 days
Burning
May be used on all skin surfaces including head, neck, and intertriginous areas Expensive
VlbiciH
PiiiiiiCrOimUI (Bidalll]
Lack& adverse 8lf8cbi of &taroid&
Ointmarrt (watar in oiU: hydrate,
Cream {ail in waf: hydra... variable lotion (powder in watar]: drying,

cosmasis Solutions {water, alcohol, propylene
glycalf
TIICIIIIimUI topical
(PrDIDpic8}
Gil (.wtian 1hlrt lllllts an cantac1 with skin]: dryinq
0.03% (children) or 0.1% Atopic dermatitis (mild to (ackllts) ointment BID moderate) Conti111e for cklration of disaBSe PUJS x 1 week after clearing
Burning Lacks adverse effec1ll of steroids May be used on all skin aurfacas including head, neck, and intertriginous areas Expensive
Toronto Notes 2011
Common Medications
Dermatology D4S
T1ble 31. Or1l Ther1pies th1t 1re Important in Dermltalogy

DIUU Name
Dosig
25-50 mg PO OD; maximum 75 mgld
Indications
Comments
Acill'ltil (Sorimne8)
SIM!rll p&oria&i& Mcnitori'll stratagia&; Other disorders of hyperkntinillltion Mcnitor lipids. LFTs at baseline and q1-Zwkun1il stable Contnjndjcatjons: (ichthyosis, Dlliar's disBBSa) Women of childbearing potential unless strict contraceptive requirements are met Drug idnctions Olhar systanic llllinoids, mathoti'BXIIIII, tatracydinas, certain contraceptives May be combined with PINA phototherapy (known as re-PUVAI
famcydovir 250 mg PO no x 7-10 days (for 1&t episode of genital harpe&) 125 mg PO BID xSd (for recurrart gerital herpes) wlecydovir 1000 mg PO BID x7-10 d (for 1&tepisode of genital harpe&) 500 mg PO BID xSd (for recurrart gl!llital herpes) 2.5-4 mwlc!Vd PO div BID Max4mg.\Wd After 4weeks may increase by 0.5 mg.\Wd qZwb Ccn:omilllrt dose of may protect the kidneys
ChiCkeiliOX Herpes zoster Genital Herpa& Acute llld prophylactic to rerilce transmission in infected patients Herpes labialis
Side eflects: Headache, nausea. diarrhea, abdomilal pain Reduce dose impaired 1111allunction
Side eflects: Dizziness, depression, abdominal pail Rerilce dose n impairad 1111allunction Drug inhn!ctiops: cimetidine Monjtorim stgtegjes Blood pressure, renal function Contraindications: Abnonnal renal function, uncontrolled hyperterlsion, malignancy {axcapt nonillelanoma skin cancar), uncontrolled infection, immunodeficiency (excluding autoimmune diseaseI, hypersl!llsitivily to drug long tl!nn eflects preclude use of cyclosporin for >2 yea11; discontinue aartiar possille May consider rotating therapy with other drugs to minimize adverse eflects of each drug Monjtorina strategies: Obtain G6PD levels before initiating; in the initial two weeks obtain levels and follow the blood coun1s carefully lor the first few months Side eflects: Neuropathy Hemolysis (V'rlilmin Cand Esupplementation can help prevent this) Drug jnb!n!ctjops: Substrate of CYP2C8/9 (minor), ZC19 (milor), 2E1 {minor), 3A4(majorl Often adramatic response within hours Monitoring strategies: Baseline lipid profile and hepatic l!llzymes befure treatment, Contmjndjcatjons Teratogenic -in females, reliable contraception is necessll'{ Generally regarded as unsafe in lactation Sjdaeff!lcb: Night blindness. decreased tolerance to contact ll!llses, dry mucous membmnes May tmnsiently exacelbate acne, dry skin Depression. myalgia DNg jnb!n!ctjons Do not use at the same time as tetr8cycline or minocycline - both may cause pseudolumour cerebri Discontilua vililmin A Drug may be discootinued at 16-20 weeks when norille coun1 has dropped by >711%. A second course may be iritiated after 2 monthspm Refractory casas may require >3 coursas Contraindications: CHF Sjda ellec!i: Serious hepatotoxicity Drug Interactions: nhibits CYP 3A4. ncmases concantration of soma drugs matabolizad by this snzyme Give capsules with food, capsules must be swallowed whole
Psoriasis May also be eflective in: Lichen Planus Dermatitis herpetiformis Erythama multifonna Recalcitrant urticaria Recalcitrant atopic dermatitis
Dlp10n1
150 mg PO OD tapering to 25-50 mg PO OD to as low as 50mg Zxlwk
Dermatitis herpetiformis
llatnltinoin (Accmne*)
0.5-1 mg.\Wclay given OD, to achi8VII a IDIBI dose of 120 mwlcg (i.e. 16-20 weeks)
SIM!rll nodular and/or inflammatory acne Acne conglobala Recalcitrant acne
llrlconllilla (SporaiiiiX*I
100-400 mg PO 00, dapencing on Onychomycosis infliction 1r8Btad Tin1111 carpori1, cruris, pedis. wrsicolor, capitis Tin corpo!Wc:ruri&: 200 mg PO OD X 7days Tinea pedis: ZOO mg PO BID x 7days Tin wrsicolor: 200 mg PO OD x 7 days Toenails with or without fingamail involvement: 200 mg PO BID x 7 days once per month, repealed 3x Fingamail involwment only: 200 mg BID PO x 7 days once par month, repaated 2x
D46 Denoatology
Common MedicationsJR.eferenc:es
Toronto Notes 2011
Table 31. Oral Therapies that are Important in Dermatology (continued) Drug Nne
lvlrmllclin
Do.ilg SdJediH
2DIJ-250 !l9"kg PO qwkly x 2 Take once as directed; repeat one week later
lndil:alion
Onchocerciasis (USA only) Not licensed for use in Canada Also effective for: Scabies Psoriasis Atopic dennatitis Lymphomatoid papLJosis May also be elfective in: Cutaneous sarcoidosis
Cummem.
No significant serious side effects IJiicacious Mgnilorioo rtnrteqies: Baseline renal, liver, and hematological studies Contraildications: Prepncy, lactation, alcohol abuse, liver dysfunction, immunodeficiancy syndrome, blood dyscrasias, hypsrsansilivity to drug Resbicted to severe, recalcitrant or disabling psoriasis not responsive to other fonns Dl therapy May be combined with cyclosporile to allow lower doses of both drugs Contn!indi!:a!ions: Caution if impaillld ranal or liver function Drug interactigns: Do not use with isCJtrelinoin {Accutane8 1 Side ef!ects: fxbnivll; affect& multiple organ sy&!BIIIs including CNS, l88th, eyes, bones, renal, ll1d skin (photosensitivity, and bkle pigmentation) Attemative to tetracycline Contraindicatians Pregnancy, chronic or active liver disease Drug interactions: Potent inhibitor Dl CYP 206; use wilh caution whan also taking beta-blockers, certain anti-an1lyllrnic agants, MAOI type B, andfor antipsychotics Drug concentrates rapidly in skin, hair and nails at levels associated with fungicidal activity Cootraindications: Severe ranal or hepatic dysfunction Pregnancy/lactation
StromadDPI
MathlllniDill
(TIIIXIP)
(Meclizln,
1D-25 mg qwk. PO, IM, or IV Max: 30 mQIWk

To minimize side effects, consider fnlic acid supplementation: 1 mg to 5 mg 6 daytlweek
Minacyclne {Minocin)
5B-100 mg PO BID Tapsr to 50 mg PO DO as acne lessens
Acnewlgaris Rosacea
Terlli111ine {Lamilil"l
250 mg PO DO x 2 weeks Fingernails x 6 wks Toenails x 12 wk.s Conlinn diagnosis prior to treatment
Onychomycosis linea corporis, cruris, pedis, capitis
Tetncyclina
251J-5DO mg PO daily Acne wlgaris Taken 1 hour before or 2hours after a meal Rosacea Bullou1 pBIIIphigoid
References
Tllllbool:l Bolognia Jl., Jori1lD J. Rapini RP, edilurs. Textboot of Demwtnlogv. Vol. land 2. Toronto: Mosby, 2003. Filzpalrict JE and Aaling JL.IlernwiDiogy Semis. 2nd ed. Phil-ia: Hlrirt & Ballus, 2001. Godelrt II, Goodheuft Phologlide Ia Cormal Slin Dillllllel$: Dillgi1Diislllld management. 3nl Edition. Uppincotl, Wiiuns and Wilijns, 2008 John11111 RA. Swiii1DIId D. Willi(, adilars. Colcur adaslllld II clinical 5th ed. Naw Yark: McGraw Kill! J, Ng C. Bllllll:ci V.lllivarsily ri TD111111D Pharmacology H111cliool: Chllptw. Toranta: 111bliCI!im panding. L.elwlohl MG, Heymann WR, l!erlhJDIU16 J, Coullon aditoJS. T1811ment ri 5ijn di1ua: 1ha11pautic $11118gia11. 2nd ad. Plilldalphia: Mo$by, 2006. Pillar AS, Mancini AJ.!Uwilz clilical pediatric darmatalogy: A18idbook of skin disorders ri mldhDDd 111d lllolllsanct. 3nl ed. Cln: Elsevier, 2006. Slllny W, Plus W. BuiQIIDII Wedilorl. Thieme Clinical Compum: llermatalogy. s1l ed, Naw York: Thieme. 2005. Wall! I(, Uld Johnlion RA. Fibpalril:t's Cobrr Atlas Uld Symop!ii II Clinicalllunnatalagy. 61h Edition. Naw York: McGraw Hill2009
Alliclll
Currvnings SR et al. AIIPIDathesto tha prMTI!ion Uld allllrol of skin cancar. Cancer Matastatis Rav. 19!7;16:309. DeShiiZD RD alii. Alaf9ie 181CtiDill Ia biologic agantJ. JAMA. 1197;278:1895. Ellis C, at ILICeAD II FWly. lnlamllilllll Can11111u Comi11nce on llllmmiliiiiiiiXAD II): Clinical updlla IIlii current tr811trrumt i!ra11Qia11. Br J llarmataL 2003; 148 j1Uppl63):31 0. J, Baron R. ciricll and diagnlllis ri onydilll11ycDiis. Br J lllrrmi 2003; 149 j1Uppl65):1-4. Friednain PS. Aaessmenl II urticaria111d 11111io-ede1T1. Cln Exper Alle!vv. 1999;29 tsuppl31:109. Gordon ML at II. Cart of the skin ltrrdl: ri pigmenlad lesions. Geriatrict. 1997;52:5667. Kllift:hik. BR. T1811ment II damwlitil. J IAJt Med Surv 3. 1989; 3!wppl2):16-23. Mlll1nllanll!a A. Urbano FG. Sailiiani l. at al A1ypical molluscum CDII!IgiDIIIII in an HN-inflctad palilnt. tit J Darma!DI. 1998; Z7:37s.380. 19111;341:964. Roujeau JC. S!Mns-Jolmson S'jlldrame and lolic necrolysis are severe variants of tile same disease Mich dillels from erythema multifonne. J Denratal. 19JI;Z74.ZJ6. Walsh SRA and Stlll8l NH.I'saliasis and the naw biok9c11Q81111: lnlarruplilg 1 T-AP danCI. CMAJ. 2004;170[13):1 933-1941. Wli1Bd JD at II. D11111 thi& paliBill hiVII mala ora1111111111n1 JAMA. 1988;Z7t-676. Wlin J,lllhl M,llalmrir M,llllb l., Fainllllin A. Odam R. Puwlll F. Stlnd1rd clusifiCIItion of RJacea: illplll ri tha Nltionlllloacaa Society Elqiart Commitlaa 1111 IIIII Clusificltion lind Stlgilg of RDIIICliL JAmar Acid llarmatal2002;46{4):584-587. Canadilllllunnatalogy AAociltion 82nd AmuiConr...:u. Juna zt.luly 4, 2007. TD!Dn!D, Ontlrio, Coneda. Pope E. Peclatric Dnthems.l.ec11Jre presenmtion to 2009-2010 lliiveiSilyofTDnllla Year 3Medical Students. hl1pi/dlrmnaln!.org
Cribier Bet II. &ytheml nodosum and assocnd di-s. lnt J Dennatal 1998;637-667.
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6 - Toronto Notes 2011 - Dermatology

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Toronto Notes 2011

l.tyen of till Epl-.15 "WomW.. Lte6etli'lg lkrl lulll$"

F"IJira 1. Crass..S.ctian Df the VariaiiS Lly.s Df Skin. Epidarmallll'(llr is datailad in A Skin

divided anatomically into epidermis, dermis, and subcutaneoWJ ti!lsue

dermiJI - comprised of ronnective tissue divided into two regions:

Toronto Notes 2011

Descrlle LIISion wllb SCALDA

Colour (e.g. hyp81Pi!rment8d,

Sldn Photolypn IFIIzpllllckJ

Table 1. Types of Lesions

Alwlys llllnt. nMr

Patch (e.g. vitiligo)

Alwlys lllln1, ltlulln

Deep Palpable (dermal or subcutaneous)

I'Hbmwn Sligllt b1111, lullr lin

Bevated Fluid-filled Lesions

Secondary Morphological Lesions

lllrkbmwn NmrU.,dllrtlln or bllck

Other Morphological Lesions

Definitions/Differential Diagnoaea of Common Presentations

Toronto Notes 2011

Patterns and Distribution

Differential Diagnoses of Common Presentations

Spider niMis Malanocytic niMIS Dysplastic niMIS Lichen planus l'$orillsis

Candidiasis Tinea inguinllis Psoriasis

'-----l'$orillsis Lichen simplex chronicus-----.../ '-----Malignant melanoma (in women) '-----Ichthyosis

Figura Z. Common Lesions Basad on Anatomical Distribution

Toronto Notes 2011

Differential Diagnosea of Common Presentations

Table 2. Differential Diagnosis of Common Presenting Proble

Diac111fB Red Papule

Folliculitis Furuncle Scabias

Acne vulgaris Lichen planus Rosacee Psoriasis Urticaria

Pityriasis rosea Secondary syphlis

Neoplastic: mycosis fungoides

Other: dermatits herplllifcrmis, paqilyria cutanee tanla

Fixed drug eruption

Autoimmune: bullous pemphi!JJS vulgaris Other: harplllifcrmis, poqilyria cutanea tanla

C!lldida Dennatophyte Impetigo Sepsis Varicalla Aspergllosis

Acne vulgaris Rosacee Dyshidllllic dermatitis Pustular folliculitis Pustular psoriasis

Acute gannlizud 8Xilllhematous (usually secondary to drug reaction)

Chemotherapy Radiation therapy

RA, Slf, vasculitis Ulcanrtiva colitis (pyoderma geniJI!Ilosum)

Common Skin Lesions

Toronto Notes 2011

Common Skin Lesions

Most common cuta1eous cyst in youth - mid age

znd most common Rare cutllleous cyst F>M

Any age 40-511% of infants

Toronto Notes 2011

Common Skin Lesions

lldn tap are lcnawn ..

Common Skin Lesions

Toronto Notes 2011

KERATOACANTHOMA Clinical Presentation

Callouses have layers at yellowish kntin FWMiad with parilg. Thare

are no thrombosed capillaries or interruption of apidannal ridges.

Toronto Notes 2011

Common Skin Lesions